The NY Times doing what it does best: waffling


The NY Times sent me an explainer for the lab-leak theory of the origin of COVID-19. It’s long. It’s very careful to present Both Sides at length. It’s what I’ve come to expect from the NY Times, a diligent, earnest explanation that gives equal weight to every position that requires some technical expertise to see through the bullshit to recognize that A) we’re in a realm of uncertainty, and B) that doesn’t mean every explanation is equally valid, and C) they’re giving disproportionate attention to a theory that has no supporting evidence. We don’t know every single intermediate step in the evolution of COVID-19, and can never know the full details of its origin, but that doesn’t imply that a claim that an intelligent Chinese designer intentionally constructed the virus in a lab.

So they cite a letter to Science signed by 18 people that says, “Theories of accidental release from a lab and zoonotic spillover both remain viable.” The letter doesn’t include any evidence. It doesn’t explain why we should consider the lab-leak hypothesis reasonable, while citing a WHO report that considers a lab accident to be “extremely unlikely”, only to dismiss it.

They cite an article in the Wall Street Journal as evidence that the lab leak hypothesis is “plausible”. Did they read the same article I did? Because that article starts with a group of Chinese miners who came down with a serious respiratory illness after collecting bat guano in an abandoned copper mine. Unless you think the Wuhan biological warfare scientists store their samples in bat shit in old caves, that only tells us that bats harbor all kinds of interesting and potentially horrible viruses, not that the viruses are intentionally created. The WSJ and the NYT do share a similar disease, though, bothsideritis. Notice the one-two punch in this short quote: first they tell us that lab origin is extremely unlikely, and then swivel to say the question divides the scientific community.

“If the world wants to shut down work that was not gain-of-function because of a conspiracy theory, that’s a huge mistake,” Dr. Daszak said earlier this year. ”This virus, it’s extremely unlikely that it came from a lab. If we focus on the lab issue and ignore what really happened, we do so at our ultimate peril.”

One question now dividing the scientific community is whether such experiments could have created SARS-CoV-2, either accidentally or as part of a deliberate effort to see which viruses could evolve into ones dangerous to humans.

I don’t think the scientific community is divided. There are a few scientists who think the lab leak hypothesis is possible and should be investigated more (but they lack any evidence), while the majority are saying “Wha…? But we already know viruses evolve rapidly, and that there are vast numbers of unknown viruses lurking in natural reservoirs, so why are you asking us to waste time on the least likely explanation?” And so it will go, round and round, with major news organizations feeding the conspiracy theories and paranoia.

Meanwhile, the strongest piece of evidence the conspiracy theorists can muster is the claim that the Chinese have been dodgy about allowing investigators in. This is nonsense. The head of the Wuhan labs, Zheng-Li Shi, explains.

Wuhan Institute of Virology (WIV), Chinese Academy of Sciences, has engaged in a long-term study on natural reservoirs of SARS-CoV[16–18] and is among the first institutions that identified the SARS-CoV-2 after the COVID-19 outbreak.[2,19] In addition, WIV discovered a virus sequence (RaTG13) that shows a 96.2% genomic sequence identity match with the SARS-CoV-2 genome, in its archived bat samples collected in 2013.[2] These results lay a foundation for understanding the origin of SARS-CoV-2, development of diagnostic methods, antiviral drug screening, and vaccine development; the findings also provide an important clue pertaining to the natural origin of SARS-CoV-2. Sadly, WIV was at the center of the misleading speculations regarding the origin of the virus, which were not fully clarified until a recent joint study was performed by an international expert team led by the World Health Organization (WHO) and Chinese experts.

The joint expert team has been working in three groups, the epidemiology, molecular research, and animal and environment groups.[20] The experts have been working together through video conferences, onsite interviews and visits, and extensive discussions. Over the course of 4 weeks, the joint team studied massive volumes of epidemic-related data and visited some facilities, including the Wuhan Jinyintan Hospital, the Wuhan Center for Disease Prevention and Control, and the Wuhan National Biosafety Laboratory (Wuhan P4 laboratory) run by WIV; in addition, they also visited the Huanan seafood market. The team interviewed local medical workers, laboratory researchers, scientists, market managers, residents, and recovered COVID-19 patients.

The joint team visited the Wuhan P4 laboratory, a facility which is the most widely speculated place of origin of the SARS-CoV-2. The Wuhan P4 laboratory is the first of such facilities to be constructed in China and runs high-level biosafety checks. The laboratory is a state-of-the-art design by French experts, jointly constructed by French and Chinese engineers and accredited by the China National Accreditation Service for Conformity Assessment (CNAS). It was designed to be a laboratory studying highly classified pathogens and an international collaboration research center on emerging infectious diseases. All activities in this laboratory on specific viruses were qualified by the China National Health Commission (CNHC). All administration and management have been strictly regulated and regularly examined and reviewed by these two Chinese authorities. It has been examined by CNAS and CNHC four and three times, respectively, since its opening at the end of 2017. Currently, this laboratory is approved to study the Nipah virus, Ebola virus, Xinjiang hemorrhagic fever virus, and SARS-CoV-2. This laboratory has played a pivotal role in fighting the COVID-19 pandemic by way of animal model studies and inactivated vaccine development, drug screenings and tests, and basic research for understanding SARS-CoV-2.

The WHO joint team has had extensive exchanges with the laboratory manager, scientists, and staff and has highly appraised the cooperation, transparency, and openness of the WIV leadership and staff. The team concluded, “They upheld a very stringent and high-quality management system. Also proceeding from the current evidence, we regard the lab leak hypothesis as extremely unlikely” in a statement released to the media on February 9, 2021, Wuhan.[5]

Shi summarizes their goals.

In the past several decades, more than 70% of emerging or reemerging infectious diseases are zoonoses and were transmitted to humans from their animal reservoirs through intermediate hosts. A huge number of unknown viruses exist in their natural reservoirs and continue to evolve, which results in the generation of new strains. Many of these viruses may have intrinsic characteristics that enable them to cross species barriers and infect humans. The rapid global economic development, including urbanization, land usage, animal domestication, and intensive agriculture, increases the chances of contact between humans and wildlife, thereby increases the risk of interspecies transmission of viruses carried by wild animals. To prevent future zoonosis, the best strategy is long-term and extensive surveillance based on science. We need to learn about unknown viruses, assess the potential risks of interspecies transmission, pinpoint the hotspots of animal-human interfaces, and eventually prepare diagnosis methods and use them for monitoring high-risk animal and human populations. With this prophylactic strategy, we can rapidly identify and limit the rapid spread of emerging pathogens at the very early stage and prevent the next epidemic. To this end, it is necessary to unify experts from different disciplines, including microbiologists, epidemiologists, veterinarians, clinical specialists, ecologists, sociologists, and policymakers, to work together on the basis of science.

Exactly. The Chinese labs are right there at the forefront of studying how zoonotic diseases emerge from animal reservoirs. It doesn’t help if, when a population is infected with a disease of natural origin, they grab the torches and pitchforks and descend in a mob on the laboratories that are trying to control the disease. Yeah, the Wuhan Institute of Virology is studying coronaviruses, because they knew these were a potential source of human pandemics; do you want to shut them down? Do you really think that an institution that was studying viruses is therefore the source of a virus?

The New York Times earned my contempt over a decade ago with their he said/she said approach to Intelligent Design creationism. They presented then their notion of balance, with long articles that highlighted creationism with equal weight to scientific studies of evolution. It drove me crazy then, and this is exactly the same thing here. The idea that the COVID-19 virus was the product of intentional design can be dismissed with a simple statement: we have no need of that hypothesis. Instead, the NY Times will quote Matt Yglesias and Tom Cotton insisting that we do, and conclude with this:

So what’s the truth?
We don’t know. Both animal-to-human transmission and the lab leak appear plausible. And the obfuscation by Chinese officials means we may never know the truth.

Let’s pretend they’re equally plausible, and then find an excuse to blame China. That’s what this was really about.

Comments

  1. says

    “Let’s pretend they’re equally plausible, and then find an excuse to blame China. That’s what this was really about.”
    That’s the way I see it. 500,000 people are dead and we lost an entire year of our lives and IT CAN’T POSSIBLY BE OUR FAULT. Chyyyyynna was Trump’s favorite whipping boy before the epidemic so of course it’s where his KKKult is going to point the finger after the epidemic.

  2. says

    My response to the hypothesis has always been ‘why does it matter?’
    Sure, it would be nice to pin down patient zero, which seems difficult to do in this situation for reasons I won’t pretend to understand, but really what changes?

    As far as I can see the lab leak does two things:
    a) Allows people to blame the Chinese, stoking that ever useful xenophobia
    b) Allows people to blame science. After all, if we didn’t study viruses, they wouldn’t exist and we could all go about our lives in blissful ignorance.

    At best, the outcome would be ‘we need to be better at securing our bioresearch facilities’, which… yes? Who is arguing for lax protocols in a virology lab? Beef up security, tighten your standards, go ahead and create an independent international organisation for the inspection and regulation of bioresearch labs. Maybe they can take a look in the basement of Fort Detrick while they’re about it.

  3. raven says

    So they cite a letter to Science signed by 18 people that says, “Theories of accidental release from a lab and zoonotic spillover both remain viable.” The letter doesn’t include any evidence.

    Cthulhu, this is stupid.
    It is an assertion without proof or data. And may be dismissed without proof or data.
    They are wrong.

  4. raven says

    This is already getting to be a dead horse people are beating up on.
    I’m just going to repost from the thread two days ago.

    What the Wuhan accidental lab release theory lacks is anything like evidence, data, and proof.

    What would really prove it would be if the Wuhan lab has the original stocks of the Covid-19 virus.
    If this theory is true, they had to have had this virus in their freezers.
    There would also be mountains of other evidence in the Wuhan lab, Covid-19 virus RNA sequences in their databases, lab experiments, lab notebooks, and so on. Genome sequencing is easy, automated, routine, and the first thing you do with a new virus isolate.

    They’ve been asked this many times, since it is the first question that would occur to any investigators.
    Wuhan has always said No. They don’t have the last known ancestor of Covid-19 virus. Or the genome sequence.

    The problem here is also obvious.
    What if they aren’t telling the truth?
    What if they did have proto-Covid-19 virus and destroyed it as part of a coverup.
    Humans aren’t very good at keeping secrets and this would be likely to come out sooner or later.
    But who knows, maybe for once, a secret remains a secret.

    I don’t completely discount the possibility of accidental release. But without proof, it isn’t very likely and not at all a useful idea.

  5. PaulBC says

    I don’t think any new evidence has moved the probability needle. Lab leak can’t be ruled out, but it’s unnecessary to assume. So my conclusion is that the new reporting is agenda-driven, the same way claims of WMDs in Iraq were agenda-driven. NYT may just want to be first with the scoop rather than actively shilling for whatever politicians are pushing this.

  6. raven says

    What we know does happen and often is animal viruses jumping to humans. We see it all the time, most recently with Swine flu, Zika, Chikungunya, and Ebola here and there.
    It happens about once every 18 months.

    The increase in animal to human jumps is because we are now 7.8 billion people. A huge monoculture that dominates the large animal biomass of the planet. It’s simple Darwinian evolution.
    We are a giant all you can eat buffet for any pathogens that are capable of jumping from animals to humans.

    This happens a lot.
    This WHO article estimates that 20 of the 30 novel pathogens found in the last three decades, came from animals.
    Most of these jumps don’t result in worldwide pandemics but like with HIV, Swine flu, or Covid-19 virus, some definitely do so.

    http://www.emro.who.int/fr/about-who/rc61/zoonotic-diseases.html

    WHO Comité régional » Sixty-first session
    Zoonotic disease: emerging public health threats in the Region 2014

    It is estimated that, globally, about one billion cases of illness and millions of death occur every year from zoonoses. Some 60% of emerging infectious diseases that are reported globally are zoonoses. Over 30 new human pathogens have been detected in the last three decades, 75% of which have originated in animals [1]

  7. raven says

    What started this whole new witch hunt off, is a report by the “US intelligence community” that a few Wuhan workers got sick and ended up in the hospital in November, 2019.
    The claim that they had Covid-19 virus symptoms isn’t in the original report.
    People keep adding that because it makes it sound more ominous.

    Well so what.
    .1. Wuhan and the Chinese government deny this even happened.
    .2. Is this report even true?
    Where is the data or proof for this allegation.
    We haven’t seen it.
    .3. People get sick and end up in the hospital all the time, especially in winter.
    It doesn’t mean they are infected with a novel pathogen.

    This is a thin reed to hang yet again, another conspiracy theory on.

  8. says

    If the intelligence community had any evidence it leaked from a lab, the pres would already have been briefed and the information would have already leaked. Therefore, the intelligence community know nothing. If they know nothing it’s probably because there is nothing to know.

  9. PaulBC says

    There’s another bait-and-switch going on here. First you say “The reason scientists were so dismissive is that they didn’t understand we meant accidental release of a natural sample. That’s a totally plausible accident, not a conspiracy theory.” Then after you regain some credibility, you slip “But I don’t know… that furin cleavage… looks kind of engineered to me.”

    One thing I wonder is if you really can rule out the plausibility of an engineered virus turning into a global pandemic. Here’s my non-biologist analogy: dog pedigrees. Let’s say you raise greyhounds to be lean and fast and run races. You know how to make them a lot better at running races than all the “mutts” around them.

    OK, so your pack of greyhound superrunners is released by accident and go feral. Do they become faster and faster in successive generations? Probably not. If any of these animals (“engineered” through classic breeding methods) manages to survive without care, their offspring will be adapted to life in the wild and more likely to resemble other feral breeds (even if they’re not hybridizing, which obviously a virus won’t do).

    So if this furin cleavage is so special that human beings and not nature had to come up with it, what’s the chance that as this virus mutates, it is going to hold onto the designed portion? It seems more likely to me that it would revert back to being like other coronaviruses. Yet we’re actually seeing mutations that are more contagious and at least equally harmful as this progresses through unvaccinated populations.

    OK, my analogy fails in many ways, but I am just skeptical that an engineered feature on a virus would have been maintained as it has over hundreds of millions of human infections. You might be able to design a feature that proves itself in vitro, but what’s the chance it keeps going this long in nature?

  10. brucegee1962 says

    We don’t know every single intermediate step in the evolution of COVID-19, and can never know the full details of its origin, but that doesn’t imply that a claim that an intelligent Chinese designer intentionally constructed the virus in a lab.

    This entire post seems to conflate “accidental lab release” and “intentionally designed virus” together as one theory, and then say that, since the second one is racist and implausible, the first is implausible as well. Surely these are theories that should be kept distinct and evaluated separately.
    There seem to be three theories up for discussion:
    1) Workers at the lab were accidentally exposed to a bat virus they were studying and infected others.
    2) The lab was trying to create a more deadly virus, and it escaped.
    3) The virus traveled from bats to humans via pangolins and infected someone using the wet market.
    We can agree that 2 has no evidence and can be discarded, but that does not do anything to affect the plausibility of 1. Lacking evidence of a specific mutation and patient zero, can we definitively say 3 is that much more plausible than 1? And also, can we all be sure that our various biases (about science, China, and governments in general) aren’t influencing our opinions?
    @3 Theories without proof or data remain worth investigating when opposing theories also lack proof or data.
    @2 Good point that, ultimately, the source doesn’t matter all that much.

  11. says

    It’s irrelevant. The government’s response was incompetent. It’s just an an attempt to shift attention. Even if it was deliberate (which would make no sense) it just shows the intelligence community is incompetent and so are all the other branches of government that should have responded in time.

    They are currently discussing the question on TWIV. I’m willing to believe their analysis.

  12. PaulBC says

    raven@8

    What started this whole new witch hunt off, is a report by the “US intelligence community” that a few Wuhan workers got sick and ended up in the hospital in November, 2019.

    True story, and I am sure many people have similar ones. I live in the SF Bay Area and my wife was tuned into this story already in early January. We were as careful as we could be, but there wasn’t really a way to alter behavior significantly.

    Some time in late February, my kids both had “flu like symptoms”. Actually I felt pretty lousy too and rarely get sick. We got over it and were fine before any lockdowns happened. We were not alone among the optimists out there wondering if we actually had just already been infected and got better. And who knows? Maybe we did.

    On the other hand, maybe our “flu-like symptoms” were… wait for it… a seasonal flu. I mean, we’re just never going to know. A lot people get sick for a lot of reasons, and I assume if it can happen to my family, it can happen to Chinese virology lab employees.

  13. says

    The real conspiracy theory would require that the intelligence community notified the president, who concealed the information.

    On Twiv: “if you mix politics with science, you get politics”

  14. PaulBC says

    As I commented in the other thread, whatever the cause of this pandemic, there will almost certainly be other similar ones of zoonotic origin, just like large fires happen whether or not Mrs. O’Leary’s cow is to blame for the Great Chicago Fire.

    From a public health standpoint, that’s what we need to prepare for instead of fixating on human agency. We should keep investigating, sure, but it won’t really matter what we find.

    The only reason to make it a priority to assign blame is to beat war drums against China. I had hoped we had seen the worst of that under Trump, but Biden may just be declaring and era of kindler, gentler Sinophobia.

  15. garnetstar says

    raven @7 is right.

    What has happened literally billions of times before? Viruses move from a reservoir into humans.

    What has happened at least a couple times? People in caves or other places that have bat guano get infected with viruses, natural transmission.

    What has never happened before on the face of the earth? A human-engineered virus “escapes” via some lab accident or lab-handling exposure or intentional release.

    Probability heavily favors the first.

  16. says

    Also on TWIV: why not worry about where Ebola comes from? We don’t know the reservoir for that, either, but no conspiracy theories about it.

  17. says

    Thanks for going over this thoroughly, PZ.

    The theories about the origins of Covid-19 are separate … and unequal. Leave it to the New York Times to add fuel to the garbage fire Trump started.

    Even after the report Biden ordered, (to be delivered in 90 days), comes to a conclusion, it will not be read carefully. Nor will it be given any credence by the cult of Trump.

  18. pilgham says

    I wish people would stop focusing on the “wet-market”. It had all the markings of a super-spreader event creating a large number of new cases, but I can’t see how it could where the jump happened. Plus we know that the disease had been around before the Wuhan market event. Blaming the lab is like blaming the firemen for all the fires. (Sometimes firemen start fires and then put them out for “practice” or “research”. hmm…).

    Plus, there is another theory that I can’t believe hasn’t been mentioned before. Some country hostile to China has the virus and releases it near the Wuhan lab to incriminate them. Of course they would have to be a pretty stupid country because the dangers of doing that are obvious, but some world leaders are just that dumb.

  19. yknot says

    I like your unintended proximity of this topic and UFOs. Just as we know of lots of explanations for UFOs, we also know of lots of ways for viruses to cross species. And just as “little green men” shouldn’t be the goto assumption for UFOs, “weaponized gain of function research” shouldn’t be the goto assumption for new diseases.

  20. says

    Chinese miners who came down with a serious respiratory illness after collecting bat guano in an abandoned copper mine.

    Now that sounds like a dangerous activity. Batshit crazy even.

  21. Pierce R. Butler says

    Marcus Ranum @ # 17: … Ebola … We don’t know the reservoir for that, either, but no conspiracy theories about it.

    Your source for that didn’t do the slightest homework.

  22. Bruce says

    To me, the conspiracy guesses seem like noting that cops and news people interview and interact with criminals. And then to conclude that the origins of crime must be the FBI and The NY Times. Equally tight “logic”.

  23. Snidely W says

    Scientific American put out a nice article about bat virus researchers in China.
    A fascinating look at their hard work:
    https://www.scientificamerican.com/article/how-chinas-bat-woman-hunted-down-viruses-from-sars-to-the-new-coronavirus1/

    One money quote:

    …estimated that there are more than 5,000 coronavirus strains waiting to be discovered in bats globally.

    “Bat-borne coronaviruses will cause more outbreaks,” Shi says with a tone of brooding certainty. “We must find them before they find us.”

  24. dstatton says

    OK, I’ve been duped. I thought that there actually was new evidence that it may have come from the lab. “Got sick” is pretty lame evidence all right.

  25. Ed Peters says

    In Yuri Deigin’s article at https://yurideigin.medium.com/lab-made-cov2-genealogy-through-the-lens-of-gain-of-function-research-f96dd7413748, he raises a lot of valid issues. I have questions. Did they destroy samples after the shit hit the fan? Have they released the lab data? Is the RRAR Furin cleavage site with the anomalous human-biased Arg codons something that needs explaining? What is the reservoir species? Were they really doing GOF experiments on SARS-COV in BSL-2 and 3? Did they do any of it in BSL-4? Yes they had the lab for BSL-4, but apparently it was not properly staffed for it, or so I’ve read. I am not familiar with Yuri Deigin or his reputation, but this piece seems honest, circumspect and thorough, and he insists we don’t have nearly enough evidence to prove anything yet. He gives lots of genetic data to chew on for those who know how to read it.

    Contrast Yuri with the Bell Curve loving science reporter Nicholas Wade, who has a piece published by “Atomic Scientists” (Yes! The perfect forum for any discipline). Nick mentions a lot of this in a more readable but obviously biased (pro-conspiracy) piece at https://thebulletin.org/2021/05/the-origin-of-covid-did-people-or-nature-open-pandoras-box-at-wuhan/. Nick’s piece is long on incendiary accusations and short on footnotes backing any of it up, and only served to get me to finally look at some of this stuff (like Yuri’s piece) instead of poo-poo-ing it, as I have done from the beginning.

    As much as I would hate for the racist conspiracy mongers to be proven right, we have to keep an open mind to new evidence that this was an accidental lab release by people who should have known to use better containment for GOF experiments. Of course, making it out to be anything more sinister is just crazy talk. As Yuri notes, this would not be the first time such a thing has happened. The US did it just a few years ago (thanks, Texas).

  26. unclefrogy says

    I keep going back to the question of why this makes a difference. How could finding a human source which seems to be the active part of this question be so attractive that it stimulates elaborate speculation and Controversy among none scientists which is so easily exploited by politicians and others with an axe to grind.
    The only thing I can figure is those who respond so “happily” and forcefully do not and can not understand nor do they want to understand just how precarious “we humans” are on this earth,
    We have through constant expenditure of energy and focus been trying to make life and the processes of the earth bend to our will. It has allowed us the illusion that we are safe from nature so the only danger like a pandemic must be from man because nature happens some where over there. It does not, after all it happens right here all the time there is no over there especially in this globally interconnected planet.
    it might also have something to do with the thinking that gave rise to the idea that we have so many cases because we are looking and counting.
    also why are we so concerned about the origin of a pandemic when it is a hoax and an exaggeration and does not exist?
    uncle frogy

  27. dorght says

    There was a documentary (Netflix?) pre-pandemic that followed scientist in Egypt and US as they collected samples from domestic livestock and wildlife in order to screen for potential infectious diseases. They used duck hunters in one case to help net and handle the ducks while the scientist took swaps. What always bothered me is that the researchers and their helpers were not taking much in the way of what we, mid-pandemic, would call pretty basic precautions.
    The question that arose in my mind then was, what if the sampling research itself is a vector for a zootronic jump to humans. I could see something like this happening in Wuhan. No evil mastermind designer required, no breech of lab safety, just the unintentional terrible consequence of well intention research. It is a possibility that deserves consideration, full disclosure, and if found to be likely to future research to be given strict guidelines.

  28. PaulBC says

    unclefrogy@29 Right. From the very beginning you could find people who could argue that it was both a hoax and a Chinese bioweapon and that somehow this was not a contradiction.

    I think that over the long term, it would be useful to find out the actual origin of the virus if possible (which it might not be). Zoonotic origin and lab accident are both things that can happen and are not necessarily blameworthy. There is no actionable distinction to be made between them, and the next pandemic is more likely to be from human-animal contact than from a lab accident. The next pandemic is the one we should be most worried about.

    However, I am sure that many China bashers are just angry that there is a lab in China to study viruses, and they are going to have their hissy fit one way or another.

  29. says

    The rapid global economic development [sic], including urbanization, land usage, animal domestication, and intensive agriculture, increases the chances of contact between humans and wildlife, thereby increases the risk of interspecies transmission of viruses carried by wild animals. To prevent future zoonosis, the best strategy is long-term and extensive surveillance based on science.

    And dramatically change our food system.

    This is an interesting thread I just came across.

    Ed Peters @ #28:

    In Yuri Deigin’s article at [blah blah blah blah blah blah blah rehashedquestionsbasedonsocalledevidencethat’sbeendebunkedazilliontimes blah blah blah…]

    Why is there someone doing this on every thread related to the virus? It’s Wade, or it’s Martenson, or it’s Deigin, and it just morphs from one conspiracy-theory form to another. What’s the SARS-CoV-2 version of bamboo in the ballots?

  30. slithey tove (twas brillig (stevem)) says

    stating the obvious after scrolling past all previous comments here. I see the common statistical error of assigning equal probability to all possibilities regardless of all conditionals. EG two targets at the end of the field, one is 100ft in diameter the other 1 foot. I take one shot blindfolded in the general direction, We hear it hits one of the targets. So it is 50 50 it hit the smaller target right, it hit one of the two. QED

  31. slithey tove (twas brillig (stevem)) says

    re @34
    html here eats dashes. 50 50 is better said as 50/50

  32. AstrySol says

    SC @ #32:

    Totally agree. The “lab-leak” camp is there JAQing to sow doubt and all this may achieve is blame-shifting and waste of time.

    Several prime examples:

    Ed Peters @ #28:

    In Yuri Deigin’s article at [blah blah blah blah blah blah blah rehashedquestionsbasedonsocalledevidencethat’sbeendebunkedazilliontimes blah blah blah…]
    Did they destroy samples after the shit hit the fan?

    It’s definitely safer to destroy potential highly-infective materials after research because people don’t want it to leak. Also, if they had kept those samples, Delgin would probably have pointed to those samples and said “See? These are the samples that leaked the virus!” and they just couldn’t win.

    Have they released the lab data?

    Where do you think all those viral sequences (that served as the basis for many of the vaccines) came from? Out of thin air?

    I am not familiar with Yuri Deigin or his reputation

    Google is your friend.

    Yuri Deigin, MBA is a serial biotech entrepreneur, longevity research evangelist and activist, and a cryonics advocate. He is an expert in drug development and venture investments in biotechnology and pharmaceuticals. He is the CEO at Youthereum Genetics and the Vice President at Science for Life Extension Research Support Foundation.

    Yuri has a track record of not only raising over $20 million for his previous ventures but also initiating and overseeing 4 clinical trials and several preclinical studies, including studies in transgenic mice.

    At Youthereum Genetics, Yuri is currently leading a project dedicated to developing an epigenetic rejuvenation gene therapy, as intermittent epigenetic partial reprogramming demonstrated great experimental results in mice: it extended their lifespan by up to 50%.

    Red flags: 1) “cryonics advocate”; 2) “epigenetic rejuvenation”; 3) MBA but self-claimed “expert in drug development”.

    Also, this guy has been beating the “lab-leak” drum from almost the beginning, so there’s that.

  33. daulnay says

    The NYT article does show something about the origins of one national problem; The Times is now an origin point of the national disease that degrades our information. It is no longer a newspaper of record, but instead a source of counterfeit information. It’s no Faux News, but is more insidious because it’s superficially accurate.

  34. bcw bcw says

    The Washington Post doesn’t do noticeably better
    https://www.washingtonpost.com/politics/2021/05/27/what-proven-coronavirus-lab-leak-theory-would-mean/

    At least they allow comments, and this was near the top:
    “Hypothesis. Not theory. Fauci did not say it wasn’t from a lab. He is a scientist. He said he was presented with no conclusive evidence that indicates it was anything but natural. Big difference from a politician. Science uses evidence to draw conclusions instead of some politicians that make claims without evidence.”

    along with some other balanced statements.

    this was mine:
    It is grossly wrong for this article to glibly conflate accidental infection of workers studying a virus in the lab with deliberate efforts to make a virus more dangerous. The accidental leak story is under consideration because it does not require extraordinary behavior from scientists. It nonetheless remains very unlikely because the lab represents just one instance of interactions between people and viruses while people interact with animal vectors constantly in markets and the wild which is how all past transmission between animals and people has happened. It is also notable that we do not know the subtext for the “three people got sick story” since the nationality and name of the source is not known. If anything, the press is too eager to embrace this lurid and sensational story now rather than having been wrong to accept the most likely interpretation earlier.

    While the virus-study-accident story has some plausibility because it is hard to prove false, there is substantial evidence against the second scenario of evil scientists making a virus. The analysis of the virus structure from early on found no evidence of human manipulation and the infection spike protein does not resemble the known highly-infectious spike proteins from other coronaviruses that humans designing a virus would be likely to make use of. In addition, the Wuhan lab does not have a history or facilities to undertake augmentation studies. You should not have implied the second scenario is possible because the first, completely different scenario has some plausibility.

  35. nomdeplume says

    Another recent piece of media “both sidesism” is the lates piece of UFO nonsense. Very similar to the covid situation.

  36. raven says

    Is the RRAR Furin cleavage site with the anomalous human-biased Arg codons something that needs explaining?

    No.
    That is just gibberish from people who have zero idea what they are talking about.

    Where do the UFO aliens come in?
    How about the Illuminati.
    The Jews must be involved with this somewhere.

    SC

    Why is there someone doing this on every thread related to the virus? It’s Wade, or it’s Martenson, or it’s Deigin, and it just morphs from one conspiracy-theory form to another.

    Because they have a captive audience.
    They can’t ramble on about their conspiracy theories to their friends because they don’t have any. Their friends long ago got sick and tired of hearing about how Trump really won the election, the grassy knoll, how the Democrats are pedophiles who drink the blood of xian children in pizza parlors and on and on and wandered off.

  37. donfelipe says

    I started seeing increased chatter about this “lab leak” yesterday and with the NY Times reporting on it I expected there was some sort of development. And by development, I mean new evidence. There isn’t, it’s all hype and paranoia. The folks who were spreading this months ago also had no evidence, and a range of implausible scenarios that none of them could agree on which degree of conspiracy we were seeing. So essentially we are in the same place, just now with more ignorant people screaming louder with even more arrogance.

    Until someone has evidence, this is all speculation by unqualified people with too much influence. But that will never stop the conspiracy theorists. They will always read hedging scientific words like “unlikely” as impossible, and won’t accept a tick in either direction as anything but proof of their conspiracy.

  38. raven says

    The people making up these conspiracy theories have no idea about what modern molecular biology/virology/medical research is or what it does**. It’s arguing from pure ignorance.

    The scary word the keep tossing around is Gain of Function. Gain of Function is no big deal and sometimes necessary to do the experiments that need to be done on pathogens. Another repost from the earlier thread.

    What the conspiracy people call gain of function studies is usually misleading because they have no idea whatsoever what they are talking about.

    We, meaning scientists, have to be able to study these viruses in order to prevent, treat, and end these pandemics. This is why we were able to come up with drugs, vaccines, and public health measures to get the Covid-19 virus pandemic under control in one year with so far only a few million dead worldwide.
    This is a major accomplishment for science and has saved many millions of lives.

    So sometimes viruses are adapted to lab conditions. Recombinants are made or pseudotypes. Sometimes viruses are adapted to our common lab animals.
    To take one example, HIV only infects humans and very inefficiently Chimpanzees. Chimps are almost never used in the labs any more.
    The virus we use to study HIV in animal experiments is SHIV. A hybrid between HIV and a Simian virus.
    Because it can infect monkeys.
    Without that, we wouldn’t have all the HAART drugs that turned AIDS into a treatable disease.

    Background. Infection of nonhuman primates with simian immunodeficiency virus (SIV) or chimeric simian-human immunodeficiency virus (SHIV) strains is widely used to study lentiviral pathogenesis, antiviral immunity and the efficacy of AIDS vaccine candidates.Oct 17, 2008
    Biomedicalcentral.com
    SHIV-1157i and passaged progeny viruses encoding R5 HIV …

    There is nothing necessarily sinister or scary about this sort of research. It’s necessary.
    This could be a disaster if SHIV ever got loose in a rhesus monkey singles bar, but that has never happened.

    What is sinister and scary and kills hundreds of thousands are conspiracy theorists who claim all sorts of nonsense about Covid-19 virus and the vaccines. Computer chips, demons, makes you sterile, shortens your life, etc.

    ** What modern medical research has done is turn HIV/AIDS into a treatable disease, drove smallpox extinct, and allowed us to get the Covid-19 virus pandemic under control in a year instead of a decade.

  39. raven says

    They used duck hunters in one case to help net and handle the ducks while the scientist took swaps. What always bothered me is that the researchers and their helpers were not taking much in the way of what we, mid-pandemic, would call pretty basic precautions.

    You are aware that many millions of people handle ducks, wild and domestic every year.

    They kill them. Pull out all their feathers. Gut them. Bleed them out, Cut them into pieces. Cook them.
    Amazingly enough they then eat them!!!
    Who knew.
    To make matters worse, these hunters and cooks aren’t wearing full suits of Personal Protective Equipment. Not even masks or gloves.

    What is more dangerous, a few researches taking swabs or a few million people hunting and eating ducks.

    (I’m not even going to get into the fisherpeople here. You wouldn’t be able to sleep if I told you what they do to trout, bass, and salmon.)

  40. Dave Booth says

    Seems to me that this is like the little Dutch boy with his finger in the dike facing an angry mob yelling that because he’s got mud on his hands he must be responsible for the flood.

  41. GerrardOfTitanServer says

    What has never happened before on the face of the earth? A human-engineered virus “escapes” via some lab accident or lab-handling exposure or intentional release.

    Note that a novel virus crossover from animals to humans as a direct result of human medical activity has happened at least once before with SV-40, and I’ll argue that it happened another time ass well with SIV. Of course, given the available evidence, I agree that the lab leak hypothesis seems to be pretty unlikely compared to the “natural crossover” hypothesis.

  42. calbat says

    And yet Shi herself says she would never expect this to happen in Wuhan in Central China. This coincidence is something a virologist when this first came to light said made his head spin. I can’t get past this bizarro world coincidence. If a virus looking like the 1918 flu broke out in Atlanta it would not be unreasonable to find out if it came out of the CDC lab.

  43. ChrisE84 says

    @GerrardOfTitanServer:
    Are you still referring to the refuted polio vaccine AIDS hypothesis?

  44. ChrisE84 says

    The arguments that it is refuted are pretty good though. The virus had developed various types at the time the vaccines were distributed.

  45. rrutis1 says

    Way upthread it is mentioned that this “investigation” will be used to beat the xenophobia drum, the side effect of this is distraction from the horrible response from federal, state, and local governments, the business community and the press (sorry if someone else mentioned this already).

    Also, does it strike anyone else as choosing the intelligence community for the investigation? I’m not saying they can’t, but wouldn’t the CDC or NIH be a better choice? Oh, that’s right, this is the same intelligence community that blew off the signs of the January 6th insurrection, ignored growing white supremecist/facist terrorism for at least 5 years but really forever and couldn’t be arsed to deny the Bush admin’s claims about WMDs in Iraq. I’d be more inclined to believe the conclusions of a bunch of 4th graders.

  46. Ed Peters says

    SC (Salty Current) @ # 32 and AstrySol @ #37

    If you know of a link where someone credible refutes whatever it is in “Yuri Deigin’s article at [blah blah blah blah blah blah blah rehashedquestionsbasedonsocalledevidencethat’sbeendebunkedazilliontimes blah blah blah…]” you are so dismissive of, I would read it. Did you read Yuri’s piece or are you just having a gut reaction becuase your mind is made up? Maybe I am not as informed as you, but I am trying to catch up, and avoid the junk, of which there is a lot to be avoided. Yuri is the best I’ve found so far. He sounds reasonable. His cryo fetish doesn’t inspire confidence, but I’m going to assume he knows more about virology than I do.

    Can you help? Do you know someone who has written a good piece explaining why the evidence so far does not point to a lab release? Someone who details what evidence is, where it came from, what the lab-accusers say is missing, whether it is really missing, etc. In other words, someone who takes the anti-lab-release position but really does a deep dive of the science. That is what I have been looking for from day one, since my initial belief was that it was not a lab release. But all I found were detailed pieces supporting the possibility of lab release. I now need more than the kind of dismissive non-responses I see here from the other side. I need to see a good detailed piece from a reputable source on the not-a-lab-release side. Have any of you seen any? Please share the links freely. Information wants to be free.

  47. Ed Peters says

    Raven @ #43 You are long on assertion and accusation, and short on facts. Not everyone who is asking questions is a conspiracy nut. If you do not accept that I am posting in good faith then I have nothing more to say to you.

  48. says

    Fuck but this is tiresome.

    First off, Ed Peters, stop perpetuating this noxious conflation: “Can you help? Do you know someone who has written a good piece explaining why the evidence so far does not point to a lab release?” Deigin is not proposing a lab release but a lab creation. These are not the same thing.

    Second, has it occurred to you that you have some responsibility to do some research on your own rather than throwing out these claims and farming the work out to other people on a blog? Have you considered that you should perhaps be more skeptical of a Medium post by a non-expert with some red flags from a year ago rather than being convinced by a superficial appearance of credibility and expecting others to marshal expert evidence against it?

    Third, as I said above, this is one of a string of threads here where this has happened. On this recent thread, “mistershelden” appears at #12 with “I realise that Nicholas Wade is persona non grata around here, and for good reason, however his survey of the evidence around an accidental lab escape is thorough and measured:…” Arguments and evidence (with links) are raised in response.

    On that thread, Rob Grigjanis and I link to previous threads where the same thing happened. Here’s one from last May, with “markme” @ #9 demanding “Can you explain how the PRRA sequence arose as pointed out by Yuri Diegin?” and asserting that “Chris Martenson has taken it further over the last week to show how it is highly unlikely that this virus could have arisen naturally….” Arguments and evidence (with links) are raised in response.

    And here’s one from last June, where “markme” again makes an appearance, as though the discussion the previous month had never happened: “The evidence for the lab origins of the virus is pretty clear. I follow Chris Martenson who has done a good job of analysing the data as it becomes available…” Arguments and evidence (with links) are raised in response.

    Go read those.

  49. Ed Peters says

    SC (Salty Current) #56 Thank you. I will read those.
    As I said before, the web is filled with junk.
    I did Google this for an hour yesterday and nothing came up except the usual SCLM junk and the few links I thought best.

  50. Ed Peters says

    SC (Salty Current) #56 Thank you again.

    Starting at : https://freethoughtblogs.com/pharyngula/2020/05/09/im-afraid-to-even-mention-plandemic/
    #26 grahamjones gave a link to: http://virological.org/t/tackling-rumors-of-a-suspicious-origin-of-ncov2019/384 posted February 7, 2020. The fact that both Wade and Deigin repeat the PRRA GOF charge without referencing it’s early debunking discredits them completely in my eyes. That was their strongest argument, IMO. I don’t even feel the need to look deeper into any of the rest of their assertions if that is the quality of their work. The world is turned right side up again.

    Sorry to bother you. Carry on.

  51. says

    Ed Peters, yeah, after I posted and read your comment again I tried to find one piece that brings together all of the various arguments and evidence in one place, but I encountered, like you said, several pages of random people “supporting” Deigin’s claims, so I understand your dilemma. I did just re-read the article I linked on the recent thread which is quite informative but unfortunately in French.

  52. GerrardOfTitanServer says

    The arguments that it is refuted are pretty good though. The virus had developed various types at the time the vaccines were distributed.

    There is no direct evidence for this. Just a circular argument, a paper that assumes its conclusion. The paper which says this assumes that there was a single crossover event and does molecular clock dating based on that assumption. If OPV hypothesis is true, multiple virus crossovers could have happened. It’s also doing dated based on rate of mutation when the particular virus changes mostly by recombination, and while they claim that they have accounted for this, they cannot have done so especially for recombination at the start where a lot would have happened on the OPV hypothesis.

  53. says

    Ed Peters @ #58, yes, I wish I understood everything in the Gallaher argument.

    This is poetic:

    Microbats, Macrobats and Bat Coronaviruses have been circulating through the Karst limestone formations in the south of China, that stretches from southeast Yunnan to western Guangdong, far longer than the Chinese people have been in existence. That is saying a lot, but it is a truth attested to by the very wide varieties found there of both hosts and viruses…Human Coronavirus disease out of that environment has been an accident waiting to happen – and still is. Emergence happens.

    About an hour from this writing, I can go on my porch and watch a flight of microbats rise from hollow trees in the wetland forest at the rear of my property, to skim the headwaters of Gum Creek for their nightly meal of insects. It is the peril of being a virologist that there are times I wonder about their virome.
    But right now, the grocery store is a far more dangerous place than my forest. We would all instinctively like to blame that on someone, somewhere. The truth is that every virus of human beings represents a past accidental emergence, an innocent wrong place, wrong time, thing.

  54. Ed Peters says

    I confess to being more than a little embarrassed by this. I had ignored this whole thing since the beginning because I believed it was nothing more than anti-vaxxers, Trumpers and racists doing what they do best. Then Biden came out with his goddam investigation speech a few days ago and by so doing, gave the nutjobs a boost. I thought “Shit. Now I have to find out for sure if there is anything there.” I am the only one in my family with a science degree (chem with biochem emphasis) and they will ask questions I don’t know the answers to. So I googled and read as much as I thought reasonable. The 1st guy, Wade, I dismissed as obviously biased. But it was harder to dismiss Deigin. He did a data dump! To my chagrin, I later found PZ’s comment about that. Anyway, so I looked at some of the data, and from what I could understand, his arguments made sense. I did note the codon frame shift in his data, but assumed (not being a virologist) that transcriptases could handle the occasional a 1-nucleotide shift. So I decided I wouldn’t waste anymore time, but come to the one place I could trust for honest brokers, here. I knew I was probably going to look like a troll no matter how supplicant I was. (I have been a lurker here since PZ was on Science Blogs). But finding the arguments that would convince me Deigin was blowing smoke, that I could share with my family, was more important than you guys thinking ill of me. Suffice it to say you did not let me down on either count :) Yes. I used you. I could have read 1.3 years of back articles on this, but I do not have that kind of time. Neither do most people. So I thank you and apologize at the same time.

    I find google is an almost useless at screening out shit. I rarely find anything I’m looking for because google delivers fertilizer in big dump trucks. Surely there is a clearing house web site of good info on COVID by now, one which has prominent pieces systematically debunking Deigin and Wade. If there is, we need to amplify it so it comes up high on any google search for COVID. Biden has opened Pandora’s box (surely he has advisors who told him the harm his speech would cause). Time to man the barricades.

    Ed

  55. John Morales says

    [OT]

    Ed:

    I find google is an almost useless at screening out shit. I rarely find anything I’m looking for because google delivers fertilizer in big dump trucks.

    There are techniques.

    Things such as: How to use search terms, how to use the engines (operators, syntax, defaults). How to see whether claims converge on a couple or sources, or whether they’re more widespread. Their consilience.
    Look for direct critiques of items you find persuasive.
    Iterate.

    (And, of course, your technique. :) )

  56. Paul K says

    I find this place to be a great clearinghouse on bullshit in regards to almost any topic. A witty, no-nonsense, take-no-prisoners clearinghouse. Thanks to all who take part! And I hope I have Ed’s courage if I ever need to ‘use’ his method of research.

  57. ChrisE84 says

    There is no circular argument here (that would have to be pointed out which ones that would be) and the conspiracy theory really needs the rejection of a lot of research, not just the timeline of confirmed AIDS cases (two cases of AIDS, not just HIV from an oral vaccine in the same year?!). You also need to reject the genetic makeup of HIV-1 types and their distribution in Africa (and the the same for SIV distribution in apes and monkeys).

  58. GerrardOfTitanServer says

    Chris.

    I just point out and describe the circular reasoning.

    I fail to see how two cases in the same year is evidence against. It’s evidence for. That amazing coincidence in time and place is one of the pieces of evidence for.

    I don’t have to reject the variation of HIV in Africa. As explained before, the analysis that you’re talking about assumed a single crossover event, aka assumed the bushmeat theory from the outset, which is the circular reasoning. The current variation could also be explained by several crossover events from a vaccine given to half a million people.

    I don’t have to reject SIV variation in chimps over all of Africa. No one claims to have tested all chimps in Africa, and furthermore we have evidence of chimps purchased and shipped from all over Africa.

    The problem here is that you want to dismiss this by labeling it as a conspiracy theory, but it’s not a traditional conspiracy theory. We don’t need thousands or millions of conspirators to explain this. We need like 5, and conspiracies of five people happen all the time.

    The other problem is that you don’t address the hypothesis as presented. You remain grossly ignorant of the fundamental aspects of the hypothesis.

  59. jack lecou says

    @67: I fail to see how two cases in the same year is evidence against. It’s evidence for. That amazing coincidence in time and place is one of the pieces of evidence for.

    I haven’t done enough research to have a dog in this fight, but I think you missed Chris’ point here. If these cases were indeed AIDS, not just HIV, and occurred in the same year as administration of this vaccine, it would rather put a crimp in the vaccine contamination theory. AFAIK, it takes untreated HIV at least the better part of a decade to progress to AIDS.

  60. GerrardOfTitanServer says

    jack
    I see. Interesting. My information is that there’s probably a 2 year gap from the first OPV vaccinations in Congo until the first known reported AIDS cases. So, not impossible.

    PS: One other piece of evidence that I forgot to mention. If the 1908 or 1920 date is correct, it’s very implausible that no physician noticed and documented any AIDS cases in the preceding decades. There would have been at thousands of infected persons. They would not have misidentified it. They weren’t stupid. Late-stage AIDS cases present in a very particular way.

  61. jack lecou says

    There would have been at thousands of infected persons. They would not have misidentified it. They weren’t stupid. Late-stage AIDS cases present in a very particular way.

    I don’t think you can assume that. Deaths from things like unexplained pneumocystis pneumonia certainly might be noted as ‘weird’ by competent coroners, but I’ve observed that an awful lot of that kind of “huh, that’s weird” can flow by, each case in apparent isolation, before enough of reaches someone in a position to notice that something systematic is going on.

    And that’s just the cases that get observed by coroners in the first place. It looks like the first “suspicious” autopsies/medical histories we’ve (retrospectively) unearthed so far (a British sailor and a Manhattan shipping clerk, apparently, both in 1959) were noted by doctors in the first-world. Which is weird, because under either theory of origin, there should have been thousands of cases in Africa at that point, or shorty after, right? So where are the piles of old autopsy reports from the Belgian Congo with notes about “weird pneumonia”? While I admit I don’t know what the public health infrastructure was like there in the first half of the century, I think we both know the likely answer. It wouldn’t be at all surprising to learn that a great many black victims died anonymously and unnoted in the 30s, 40s and 50s, possibly without even the courtesy of a death certificate, never mind a proper autopsy.

  62. GerrardOfTitanServer says

    I think we both know the likely answer.

    I know the answer. You don’t. The Congo at the time had a great medicine infrastructure,
    https://www.tandfonline.com/doi/abs/10.1080/02665433.2019.1633950?journalCode=rppe20

    which IIRC was one of the big reasons why Koprowski chose the Congo and its population as the location of his medical experiments, aka trial runs of his new OPV vaccine.

    And from what I know, I still disagree: late-stage AIDS presents very specifically and uniquely. It’s not just pneumonia. It’s very often a certain combination of certain diseases, IIRC like 3 or 4, that appear together which basically never happen in healthy adults. That’s how the USA found out about it during the initial outbreak in the San Francisco gay population. IIRC, the initial cases in the USA, because of their very unique nature, raised all sorts of flags with the doctors, and the doctors immediately knew that they were dealing with something new. Somehow missing one or two late-stage AIDS cases in the Congo, that’s understandable. But passing over 10s, 100s, maybe 1000s, over several decades, in a country with what was a modern and advanced medical infrastructure? It’s not plausible.

  63. GerrardOfTitanServer says

    a British sailor

    Wasn’t AIDS. At least, no hard evidence that it was.
    https://en.wikipedia.org/wiki/Timeline_of_early_HIV/AIDS_cases
    Based on later testing, the initial positive result was probably in error, and the initial positive result seems like it was lab contamination. And even if it was AIDS, that can still fit the OPV hypothesis timeline.

    As for Ardouin A. Dunno. No HIV testing was done. Maybe just a fluke. Maybe AIDS. I don’t know enough of the history offhand to know what direct and indirect contacts might have existed between him and the Congo.

  64. jack lecou says

    I know the answer. You don’t. The Congo at the time had a great medicine infrastructure,

    If that’s the case, then why didn’t anybody notice AIDS until the 1980s. In the first world.

    The point is, you’re saying: if the natural crossover at the beginning of the century was true, somebody would have noticed AIDS cases in the 1930s or 40s, maybe in the Congo or another epicentre. AIDS is just too obvious.

    But by the same token, if a contamination hypothesis is true, and AIDS is so easy to recognize, then somebody should still have noticed all those vaccine transmitted AIDS cases in Africa first, albeit starting a couple decades later.

    They didn’t. Either way, we know there were thousands or tens of AIDS cases in Africa that didn’t get noticed. Whatever the reason for that, it’s clear that it was possible. It’s a pretty weak argument against the earlier natural crossover hypothesis.

    Wasn’t AIDS. At least, no hard evidence that it was.

    Not the point. Whether those were caused by HIV or not, the point is that the symptoms are the kind of thing doctors and coroners should have been noticing in an AIDS outbreak, if they were going to. Yet they didn’t, in Congo or elsewhere in Africa (not enough, anyway), even half a decade later when the vaccine-induced cases really should have been cooking off. Meaning that HIV, whenever it was introduced, could and did go unnoticed in Congo.

  65. GerrardOfTitanServer says

    But by the same token, if a contamination hypothesis is true, and AIDS is so easy to recognize, then somebody should still have noticed all those vaccine transmitted AIDS cases in Africa first, albeit starting a couple decades later.

    Why do you think that they didn’t? Why do you think that American doctors were the first to notice this new disease? Because they were the first ones to give it a name? Before being discovered by American doctors, HIV-AIDS was well known in Uganda as a new and horrible disease in 1980 called “Slim”. There is clear testimony from doctors of widespread AIDS in parts of Tanzania in 1981. Zambia in 1983 (a 10x increase in Kaposi Sarcoma cases in one hospital, along with other evidence). Doctors in retrospect say that the disease was rampant in parts of Congo in 1974. Certain other evidence pushes this back even earlier, to 1970 at least. This is not a disease which can be easily ignored when it’s so widespread. Doctors and hospitals are going to notice, and they did notice. If HIV/AIDS did exist in humans before circa 1960, it must have been exceedingly rare.

  66. jack lecou says

    HIV-AIDS was well known in Uganda as a new and horrible disease in 1980 called “Slim”. There is clear testimony from doctors of widespread AIDS in parts of Tanzania in 1981. Zambia in 1983.

    Right. This is my point.

    We don’t have to hypothesize about what kind of disease levels would have reached the notice of health authorities. We know exactly what the threshold was. It was whatever the levels were a couple years either side of 1980. I don’t know if anyone has estimates for how many thousands (millions?) of people were living with HIV/AIDS in central Africa at that point, but it was obviously very, very high. “Number of infected per 100 people” high, rather than per thousand or per million. When a disease reaches the point where it’s not just getting noticed in passing by coroners every few years, but actually has its own terrifying slang nickname, it’s reached a horrific level which is more accurately described as “can’t be ignored” than “will surely be noticed”.

    This is just history.

    But…the point you made earlier was that if HIV had crossed over sometime prior to the 50s, “…it’s very implausible that no physician noticed and documented any AIDS cases in the preceding decades. There would have been at thousands of infected persons. They would not have misidentified it. They weren’t stupid. Late-stage AIDS cases present in a very particular way.”

    And yet, looking to the history above, we see that’s exactly what must have happened at some point or another. For the epidemic to reach the horrific level it had by 1980, thousands of cases must have been misidentified or ignored throughout the 60s and 70s. Sure we have a few retrospective identifications, now, thanks to reviews of old records, but surely only a fraction of them. I’m sure every doctor you ask about that will say “oh yeah, there must have been a lot more we didn’t catch.”

    So if, say thousands of cases were being missed in the 70s and 60s, is it actually so implausible that hundreds of cases were being missed in the 50s? That tens of cases were being missed in the 40s (with a war on, no less)?

    I’m no epidemiologist, but I think your reasoning on that point is…shaky. And the fact that real epidemiologists don’t think it presents much difficulty to the natural crossover theory should also give you some pause.

  67. GerrardOfTitanServer says

    I’m no epidemiologist, but I think your reasoning on that point is…shaky. And the fact that real epidemiologists don’t think it presents much difficulty to the natural crossover theory should also give you some pause.

    Do they? As far as I can tell, the number of academics that publish on this issue I can count on two hands. Do you actually know that a lot of epidemiologists have looked at this in detail and there is a proper scientific consensus? Because I don’t think that there is. There’s a group in the neighborhood of 5 people, half of which were part of Wistar Institute with Koprowski, who work and publish on this.

    So if, say thousands of cases were being missed in the 70s and 60s, is it actually so implausible that hundreds of cases were being missed in the 50s? That tens of cases were being missed in the 40s (with a war on, no less)?

    Were they missed? Were there thousands of cases that were missed for 50 years? You’re assuming that’s true. I’m perhaps suggesting that it’s not. I’m suggesting that the outbreaks in each country were noticed within a few years, at most a decade, after the start of intra-community spread in the local population. People have gone looking through the medical records, and while there are a few rare cases of an otherwise healthy adult with AIDS-like symptoms, they’re quite rare, and Hooper has gone through many of them, including the ones mentioned above, and given plausible alternative explanations, like berylium poisoning on the job for Ardouin A., based on interviews with doctors, friends, and family. HIV/AIDS could not remain undetected for long if it was at high levels.

    I say again, the cut-hunter hypothesis is simply not believable. The cut hunter hypothesis says that one person was infected circa 1908 or 1920, infected in a country that was several countries away from the epicenter of the pandemic, Congo. (Based on the mainstream supposition that we’ve identified the likely chimp population that carried the immediate SIV precursor to HIV.) You then have to believe that the infection did not die out e.g. at least one infected person remained to keep the infection going while also believe somehow that the number of infected stayed low enough in any one area so that the local hospitals and doctors wouldn’t notice it. Worse, based on the phylogenic dating argument which is the basis of the 1908 or 1920 or whatever date, you have to assume that half a dozen separate viral infection chains independently stayed alive in the human population starting circa 1908 or 1920, and they simultaneously reached the Congo circa 1960 to start the outbreak, traveling across several countries to get there, and none of them starting an outbreak before 1960 and none of them starting an outbreak in a country other than Congo. Why did they all join up in Congo circa 1960 to start the pandemic? Why not one in South Africa and another in Zaire? Why not an earlier infection in Europe or Asia? Why did the separate strains all start wildly spreading in 1960 instead of a decade earlier or a decade later? This is the mainstream hypothesis with a generous presentation. When you actually write it down, it’s actually quite absurd. It’s incredibly implausible that so many separate chains of infection could remain below pandemic levels, and not die out, and yet all start pandemic spread at the same time and same place about 50 years later and in a country that was 2 countries away.

  68. says

    @ jack lecou and anyone else that actually cares

    It seems the link I provided earlier was lost to the noise. I’ll give it again:
    https://www.historyofvaccines.org/content/articles/debunked-polio-vaccine-and-hiv-link
    Anyone actually caring about this topic should at least read it. If you care even more, go on to read primary and secondary literature it cites. Even more, go to pubmed and search for the numerous publications on HIV’s origin.
    HIV is the virus most studied by humanity so far, including its origins. The field consensus is that HIVs are the result of zoonosis. The anti-vax conspiracy theory is just that, no evidence for and stacks against.

  69. KG says

    The question that arose in my mind then was, what if the sampling research itself is a vector for a zootronic jump to humans. I could see something like this happening in Wuhan. – droght@30

    The researchers at WIV go into bat caves all over China to collect samples (see Snidely W.’s link@26). They do use PPE, but there must still be some risk of infection, and not necessarily by a virus from a collected sample – the air in those caves must be loaded with any respiratory viruses the bats are infected with. Apparently farmers also go into such caves to collect guano for fertiliser, but I’ve read there are no such caves near Wuhan, and it certainly seems a remarkable coincidence that the first city affected was the one containing China’s only level 4 biosafety lab, known to be collecting samples from bats and working on bat coronaviruses. I thought early on this was a likely source of the pandemic, and I still think so – but we’ll probably never know. Research on dangerous pathogens is always a two-edged sword.

    As for those saying it doesn’t matter it sure as hell matters for the Chinese government. If they know or suspect the virus did in some way get into the population as a result of WIV’s work, they are certainly not going to tell us, so their denials mean nothing. Most governments would probably act the same, but we do know the Chinese government lies systematically (e.g about their persecution of the Uighurs).

  70. KG says

    But passing over 10s, 100s, maybe 1000s, over several decades, in a country with what was a modern and advanced medical infrastructure? It’s not plausible. – GerardOfConspiracyTheories@71

    Your own link says the hospital infrastructure was being built in the 1950s. This was a late-colonialist attempt to justify continuing Belgian control. And infrastructure doesn’t constitute a health system. You need trained staff, medical supply chains, and for that matter a population that is in the habit of coming to the hospital when sick. Did all those things exist in the Congo of the 1920s-1940s?

  71. Rob Grigjanis says

    KG @78:

    it certainly seems a remarkable coincidence that the first city affected was the one containing China’s only level 4 biosafety lab

    I’m not sure it’s that remarkable. Wuhan is also a vast metropolis and high-speed train hub.

  72. GerrardOfTitanServer says

    KG

    We have testimony from doctors working in the area that they noticed the outbreak in Congo circa 1975, and same and other doctors working in the same area who testify that they saw no such thing before 1960. Yes, they would have noticed, especially in the later years before 1975 when they actually started noticing something.

    D

    It seems the link I provided earlier was lost to the noise.

    It also seems that you didn’t read any of the obvious rebuttals.

    https://www.historyofvaccines.org/content/articles/debunked-polio-vaccine-and-hiv-link

    First, leftover stocks of the polio vaccine in question were examined by independent laboratories, and were confirmed to have been made using monkey cells—not chimpanzee cells, as Hooper had claimed. Furthermore, none was contaminated with HIV or SIV. This data reinforces the vaccine developers’ statements that only monkey cells, not chimpanzee cells, were used in producing the vaccine.

    They tested original vaccine made in Europe, and not vaccine amplified in Congo. Therefore, the test is irrelevant. The early first version of the theory says that the original creation in Europe was contanimated, but this was revised into the second verison of the hypothesis based on later investigation and evidence which showed that the contamination probably happened in Leopoldville, Congo, during local amplification of the vaccine. There has been no tests of any OPV vaccine that was actualy present in Congo.

    Second, a 2004 study published in Nature found that the strain of SIV affecting chimpanzees in the area where Hooper claimed vaccine had been prepared using chimpanzee cells was genetically distinct from HIV strains. This refuted Hooper’s claims from yet another angle: even if SIV-infected chimpanzee cells from that area had been used to make the vaccine, they could not have been the source of HIV.

    We haven’t tested enough chimps to be sure of this. Second, we have evidence of chimps being brought from all over Africa.

    Epidemiological studies also highlight a serious problem with Hooper’s claims of an OPV/HIV link: HIV-1 (the first of two known species of HIV, more infective and virulent than the second, HIV-2) was likely introduced to humans prior to 1940, and in a completely different part of Africa than the location of the polio vaccine trial, probably via infected chimpanzees in Cameroon. The Congo vaccine trials took place in the late 1950s—at least a decade after HIV had begun spreading in humans, and probably longer, according to more recent estimates (Worobey 2008). The vaccine could not have been the source of a virus that had already been infecting humans for many years.

    A bit of circular reasoning. It assumes the cut-hunter hypothesis in order to make the dating argument which concludes that it must be the cut-hunter hypothesis. It assumes a single virus transfer. By contrast, under OPV hypothesis, where half a million people were potentially exposed, there could have been several points of transfer.

    The entire paper is also fatally flawed. It’s doing dating on an RNA retrovirus under the assumption of a constant rate of mutation, but this RNA retrovirus changes primarily through recombination, and in spite of a few words in the paper that it accounts for it, it really can’t.

    Hooper, for his part, stands by his claims and alleges an organized cover-up, but his argument has largely been relegated to the status of a debunked conspiracy theory.

    Sometimes conspiracies happen. Especially when the conspirators are very small in number and stand to lose if the truth comes out, which is what we have here. Calling it a “conspiracy theory” is an ad hom cop-out instead of properly rebutting the argument. It’s conflating the implausibility of 1- a conspiracy of thousands or millions of people, typical “conspiracy theories”, with 2- conspiracies of 5 business partners which happen all the time.

    Yet even though his claims have not been found to have merit, they have still managed to damage global efforts to eradicate polio. Rumors of the current oral polio vaccine having been intentionally contaminated with drugs to cause sterility and “viruses which are known to cause HIV and AIDS” led to local refusals to accept the vaccine in parts of Africa. It’s likely that these rumors are related to the original OPV/HIV accusations. Partially as a result of these refusals, polio flared back up in parts of Africa after vaccination had led to positive steps toward eradication.

    This is not an argument to avoid seeking the truth. This reeks incredibly of paternalistic and colonialist thinking, “I know better than you, and you should do what I say”. It’s this sort of sentiment which further feeds the real oppression and persecution narrative in Africa and other former colonies.

    All of the supposed disproofs of the OPV hypothesis are nakedly transparent and without merit.

    D:

    The field consensus is that HIVs are the result of zoonosis.

    Is it? There’s like 5 people who work and publish on this topic. Saying that there is a scientific consensus against it seems to me to be without any basis in facts. What evidence do you have that there is a large number of relevant scientists who have sufficiently looked at the idea and said that it’s wrong?

    Anecdotal hearsay evidence suggests that it has more support from academia but they don’t want to voice their tentative support for fear of losing their careers. Just look at what happened to the guy who exposed the universal HeLa cell culture contamination problem. They ruined his career.

    The academia plus private medical industry is not the most trustworthy thing, especially when we’re talking about how cavalier and unregulated it was back in circa 1950. Just read about the widely accepted things that they did back then, especially Koprowski. You’re really going to rely so heavily on the honesty and integrity of some shady white capitalists who unethically experimented on mentally handicapped children in Europe and unethically experimented on practically forced “volunteers” in colonial Africa? Koprowski is scum. AFAIK, he was kicked out of his former employment for ethical issues, including some of the abuses named above, and he left and took some staff with him to Wistar where he made his CHAT OPV. These are demonstrably not good people, and trusting their honesty is foolhardy.

  73. jack lecou says

    @76
    Were they missed? Were there thousands of cases that were missed for 50 years? You’re assuming that’s true.

    No. We know for a fact that’s true.

    You keep conflating detection of an outbreak with detection of the individual cases. And the outbreak was eventually detected, sure. But a lot of cases weren’t. Are you really saying that we have records for every case between 1960 and 1980, even retrospectively? Of course not. We have a tiny handful of cases, mainly found by combing through old records. What’s that as a fraction of the infections that were actually present in the population? Tiny. Thousands of cases were missed. That not’s even debatable.

    And given that the infection level and disease rate would have been exponentially lower back in 1950…1940…1930, and levels of contact with the medical community were simultaneously likely to have been poorer the further we go back (and other factors probably contributed to increased transmission rates in the 50s and 60s), I don’t think it’s at all stretching credulity that we haven’t (yet) uncovered any one of the likely tiny handful of suspicious medical histories that might ever have been recorded in say, the 40s. Insisting that these should have been found by now is just a very unconvincing argument on your part.

    It also seems increasingly clear that if one or two such cases were to be uncovered, you’d be more than ready to discount them as something else. (While simultaneously claiming that AIDS symptoms are unmistakable…)

    This is the mainstream hypothesis with a generous presentation.

    That actually sounds like rather a lot of misrepresentation. Your version only superficially resembles the story told in this paper, for example. You’re mainly just throwing in a lot of incredulous editorializing that (much like the “they would have noticed” argument) doesn’t seem to be backed up by much.

  74. jack lecou says

    @78:
    Apparently farmers also go into such caves to collect guano for fertiliser, but I’ve read there are no such caves near Wuhan, and it certainly seems a remarkable coincidence that the first city affected was the one containing China’s only level 4 biosafety lab, known to be collecting samples from bats and working on bat coronaviruses.

    I don’t know about caves, but there are certainly still bats in Wuhan (well, Hubei province, anyway), including the horseshoe bats where SARS-CoV-2 relatives have been found. Caves aren’t the only place that bats can live, and Hubei has plenty of trees and barns and so forth.

    But also, the hypothesis is not necessarily that it came directly from bats. Bats get a lot of blame because they’re very stable long term ultimate reservoirs of these viruses, but the chain of transmission to humans can and does often involve intermediate hosts that bridge the gap to humans, both immunologically and geographically.

    Indeed, in the case of SARS-CoV-2, it couldn’t have come directly from the Hunnan bats where the closest related virus has thus far been identified — it’s just not close enough. There was certainly some other as-yet-unidentified intermediate host, maybe another group of bats, maybe some other animal, maybe both, where several decades worth of additional mutation occurred. Since we don’t know what that animal is yet, we certainly don’t know whether it has a habitat in or around Wuhan.

    Also:
    Coronavirus research is usually done in mere BSL-2 and BSL-3 labs. BSL-4 is for Ebola and stuff.

    And there are ~50 or more BSL-3 labs in China, sprinkled all over the country. There’s even another BSL-4, in Harbin. And probably hundreds of BSL-2s. I’m not sure there’s any city in China where an outbreak could start and you wouldn’t be able to find a lab across town or just up the road somewhere that’s potentially doing coronavirus research. It’s just really not as much of a coincidence as you might think.

  75. says

    I see Gerrard is heading to full crackpot. I’m not going to bother with the bulk of the baseless claims and non-sequitors. For the possible benefit of people reading, however:

    They tested original vaccine made in Europe, and not vaccine amplified in Congo. Therefore, the test is irrelevant.

    The Congo site did not produce/amplify the vaccine at that time (follow those links to the primary lit if you want to read all the details). That is a baseless claim by the author of the conspiracy theory. There is no record or mention of such happening at the Congo location otherwise and all those that could have been involved deny it happening. But it wouldn’t be a grand conspiracy if a lack of evidence and people denying it weren’t taken as evidence of the grand conspiracy. And lets be clear, if there was actual evidence of this conspiracy theory, hundreds if not thousands of people would have to be in on it, the primary researches/health professionals at the time to the vast number of people that have investigated it since. Here are some of those investigators and their work regarding the origin of HIV-1.

    Zhu T, Korber BT, Nahmias AJ, Hooper E, Sharp PM, Ho DD. An African HIV-1 sequence from 1959 and implications for the origin of the epidemic. Nature. 1998 Feb 5;391(6667):594-7

    Gao F, Bailes E, Robertson DL, Chen Y, Rodenburg CM, Michael SF, Cummins LB, Arthur LO, Peeters M, Shaw GM, Sharp PM, Hahn BH. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes. Nature. 1999 Feb 4;397(6718):436-41

    Korber B, Muldoon M, Theiler J, Gao F, Gupta R, Lapedes A, Hahn BH, Wolinsky S, Bhattacharya T. Timing the ancestor of the HIV-1 pandemic strains. Science. 2000 Jun 9;288(5472):1789-96. doi: 10.1126/science.288.5472.1789

    Hahn B.H., et. al.: AIDS as a zoonosis: scientific and public health implications. Science 2000; 287: pp. 607-614

    Worobey M, Gemmel M, Teuwen DE, Haselkorn T, Kunstman K, Bunce M, Muyembe JJ, Kabongo JM, Kalengayi RM, Van Marck E, Gilbert MT, Wolinsky SM. Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960. Nature. 2008 Oct 2;455(7213):661-4

    Hemelaar J. The origin and diversity of the HIV-1 pandemic. Trends Mol Med. 2012 Mar;18(3):182-92

    Rife B, Salemi M. On the early dynamics and spread of HIV-1. Trends Microbiol. 2015 Jan;23(1):3-4. doi: 10.1016/j.tim.2014.11.004. Epub 2014 Nov 20.

    Faria NR, Rambaut A, Suchard MA, Baele G, Bedford T, Ward MJ, Tatem AJ, Sousa JD, Arinaminpathy N, Pépin J, Posada D, Peeters M, Pybus OG, Lemey P. HIV epidemiology. The early spread and epidemic ignition of HIV-1 in human populations. Science. 2014 Oct 3;346(6205):56-61

    I could go on (a fair bit more than 5 people, or maybe I’m bad at counting). All of those place the start of pandemic HIV at least a decade, if not much more, prior to the vaccinations, based on the observed phylogeny and observed rate of HIV-1 mutation. None of them require a prior conclusion as to the source of that origin.

    I’ll reiterate again. If anyone actually wants to understand this for themselves, go to the primary literature and actually read it (it is clear Gerrard either hasn’t or greatly misunderstands it).

  76. jack lecou says

    Apropos of nothing, here’s a a cave in Wuhan.

    Obviously this particular one is a paved, heavily trafficked tourist attraction, so I don’t know if it’s very bat friendly. But the local geology clearly allows for it. Where there’s one, there’re probably more.

    I think it goes to show we all need to be careful about casually accepting claims like “there are no caves in Wuhan”. There are a lot of people pushing lies and rumors right now – question everything.

  77. jack lecou says

    Apropos of nothing, here’s a a cave in Wuhan.

    Obviously this particular one is a paved, heavily trafficked tourist attraction, so I don’t know if it’s very bat friendly. But the local geology clearly allows for it. Where there’s one, there’re probably more.

    I think it goes to show we all need to be careful about casually accepting claims like “there are no caves in Wuhan”. There are a lot of people pushing lies and rumors right now – question everything.

  78. GerrardOfTitanServer says

    The Congo site did not produce/amplify the vaccine at that time (follow those links to the primary lit if you want to read all the details). That is a baseless claim by the author of the conspiracy theory. There is no record or mention of such happening at the Congo location otherwise and all those that could have been involved deny it happening.

    It was standard practice to amplify the vaccines locally. Nurses working there testify on camera that they sacrificed hundreds of chimps and got their kidneys. There is evidence of hundreds of chimps being shipped to the lab in Congo and being killed. There is no reason for such an extremely high number of chimps being sent to a lab in the middle of nowhere and killed unless they were being used to amplify the vaccine.

    And lets be clear, if there was actual evidence of this conspiracy theory, hundreds if not thousands of people would have to be in on it, the primary researches/health professionals at the time to the vast number of people that have investigated it since.

    What are you talking about? How many people have investigated this? It’s not hundreds. It’s like 5. If you want to point me to primary sources or persons who did investigate this who were not directly involved with Wistar, I’d like to know.

    I could go on (a fair bit more than 5 people, or maybe I’m bad at counting). All of those place the start of pandemic HIV at least a decade, if not much more, prior to the vaccinations, based on the observed phylogeny and observed rate of HIV-1 mutation. None of them require a prior conclusion as to the source of that origin.

    These people did not investigate whether CHAT OPV was amplified locally in Congo. These people don’t need to be in on the conspiracy. I’m not claiming that they are. Only a few business associates of Koprowski and Wistar need to be directly involved to lie about the use of chimps for local amplification in Congo.

    What these other authors is doing is something different. These other authors that you cite are making the same debunked phylogenetic dating argument. Maybe they’re aware of the CHAT OPV HIV/AIDS hypothesis. Maybe they’re not. I don’t care enough to read them because from their titles it seems most if not all are making the same fundamental errors that I mentioned above, which means that their results are not relevant to this discussion. If you want to at least pretend to engage with my actual arguments, I’ll be here.

  79. GerrardOfTitanServer says

    D
    Here. Let me say it again for your benefit. These papers are assuming the cut-hunter hypothesis to be true as a starting assumption for their dating methods. In other words, they’re assuming that there was a single viral crossover from chimps to humans. In other words, they’re excluding the possibility a priori of a punctuated event, of multiple crossovers at about the same time, which is plausible if not likely on the CHAT OPV hypothesis. In other words, using these papers to debunk the CHAT OPV HIV/AIDS hypothesis is simply an exercise in circular reasoning.

    And that’s before we get into the fatal methodological problems of dating by constant mutation rate for a virus that changes primarily by recombination.

    Finally, I’m no expert, but it’s also my understanding that the HIV phylogenetic tree is quite unusual. It’s a starburst pattern. That’s highly unusual. Almost always genetic trees have a different form where there’s a split, and then one of the branches splits again, and another branch splits again, etc. This is very different from the starburst pattern where much of the branching happens in a single point on the tree (hence the name “starburst”). This is suggestive that we don’t have normal evolution happening here. This is suggestive that we have something highly unusual – such as 400 chimp kidneys being used to create cell cultures to amplify a vaccine that was given to half a million people. This explanation perfectly fits the highly unusual starburst-shape of the HIV phylogenetic tree, and the cut-hunter hypothesis cannot.

  80. John Morales says

    Gerrard, ahem.

    And lets be clear, if there was actual evidence of this conspiracy theory, hundreds if not thousands of people would have to be in on it, the primary researches/health professionals at the time to the vast number of people that have investigated it since.

    What are you talking about? How many people have investigated this? It’s not hundreds. It’s like 5.

    Talking about the people who would have to be part of the conspiracy you allege, not those who investigate whether it exists.
    Explicitly so: “Here are some of those investigators and their work regarding the origin of HIV-1.”

    I note 8 citations were provided as a limited sample (“I could go on (a fair bit more than 5 people, or maybe I’m bad at counting).”).

  81. GerrardOfTitanServer says

    John
    If you want to engage with what I’ve actually written, I’ll be here.

  82. John Morales says

    BTW, in the news today:
    Mouse plague control hopes raised with funding for genetic biocontrol research

    The New South Wales government has today announced a $50 million mouse control package which includes $1.8 million dollars in funding for genetic control of mice populations.

    The project aims to fast-track the delivery of next generation “gene drive” technology to control plagues of the future.

    Researchers have welcomed the announcement, including Australia’s lead researcher Professor Paul Thomas from the University of Adelaide.

    He said the technology is only relatively new, having been developed to some extent for insects and malaria control, but has not yet been applied to mammals.

    “So effectively it just uses the natural mating processes to spread a gene though a population that will cause, [and] what we are trying to cause, female [mouse] infertility,” he said.

    (What could possibly go wrong?)

  83. jack lecou says

    It was standard practice to amplify the vaccines locally. Nurses working there testify on camera that they sacrificed hundreds of chimps and got their kidneys. There is evidence of hundreds of chimps being shipped to the lab in Congo and being killed. There is no reason for such an extremely high number of chimps being sent to a lab in the middle of nowhere and killed unless they were being used to amplify the vaccine.

    That all sounds like it’s been rather well covered long ago. As an aside, this conspiracy is pretty bonkers. Apparently, they can’t even decide on which continent the nefarious vaccines are supposed to have been made. The phrase “while accusations” comes to mind.

    Here’s a (long but interesting) excerpt relevant to the discussion above about the detectability of early cases. Could have saved some time if I’d read this sooner:

    <

    blockquote>Were there AIDS cases before 1959? The River argues that the absence of confirmed HIV infections or AIDS before 1959 is a strong argument in favor of the polio vaccine hypothesis. However, medical care was in general available in the Congo only in towns. We know from analysis of the data that infection was rare before 1970. In that year, the prevalence of HIV infection was only 0.2% among pregnant women in Léopoldville, but it rose to 3% 10 years later [50]. Auvert et al. [51] plotted the epidemic curve for Léopoldville. They back-calculate that the number of infected individuals already exceeded 10 in Léopoldville in 1952 ± 5 years, placing the introduction well before the first OPV vaccination.

    Moreover, it is well known that the first serum to test positive for HIV antibodies was obtained early in 1959 by Arno Motulsky in Léopoldville [52–54]. Although the serum came from an adult, only children were vaccinated in Léopoldville. Several explanations of how this could have been a vaccinated individual are offered in The River. However, Motulsky also collected 98 specimens from adults in Stanleyville, 116 children in Bukavu in Ruzizi Valley, and 99 children in Nyanza. All of those are places where CHAT vaccination was conducted in 1957–1958. Nyanza is particularly interesting because vaccine was given there during the campaign that was suspected to have been from a contaminated lot (see section above, “Vaccination in Burundi”), yet none of the serum specimens was positive. Although the numbers are small, these are striking negative data.

    Whereas the absence of known HIV-positive patients before 1959 cannot prove or disprove an association between infection and CHAT vaccination, one can certainly say that there is no epidemiological resemblance to a common source outbreak. The specimens collected by Motulsky in 1959 yielded only 1 positive result in 500 specimens, and in 1970, only 0.2% (1 in 500) of pregnant women in Léopoldville yielded positive results [50].

    The combination of rarity of infection, perhaps confined to individuals in rural areas, plus the lack of medical care in those areas would have allowed isolated illnesses and deaths to pass unnoticed. Moreover, the fact is that AIDS in the Congo went unnoticed for over 20 years (from the early 1960s to 1983), even as it was becoming more prevalent. Even in the United States and Europe, where AIDS cases go back to at least 1974, the disease went unrecognized until 1981. A case of possible AIDS seen in Léopoldville in 1962 [55] is mentioned in The River, and an attempt is made to link it to CHAT vaccination in Lisala in 1958. However, the case history related in the book shows that the woman was already symptomatic in 1958. Moreover, a later study [56] showed that HIV seroprevalence was not higher in Lisala than in Bumba, where vaccination had not been done.

    Two longtime African observers commented to us on the possibility that AIDS could have gone undetected in Africa for many years. In a letter to me dated 6 March 2000, Dr. Michel Garenne writes:

    Is it likely that an unidentified disease could be noticed by colonial physicians before 1959, the date of the first documented HIV/AIDS death in tropical Africa? The answer is clearly yes, and there are many arguments for this statement, assuming that HIV/AIDS was sporadic before that date. First, several very lethal tropical diseases, which most likely existed before, were discovered after 1960, such as Lassa fever (1969) and Ebola (1976). These diseases were identified in towns where colonial hospitals or clinics had been functioning since the mid-1930s.

    Second, even very well known lethal diseases, such as measles and whooping cough, were ignored by colonial physicians before 1960. One of the first colonial reports on medical geography argued that measles did not exist in tropical Africa outside of imported cases along the coast.

    In an e-mail to me dated 15 February 2000, Dr. Philippe Van de Perre commented, “In fact, I think that certain cases of AIDS could have passed unperceived for a long time. During my first sojourn in Kigali (Rwanda), of all the cases that I reviewed in the first article published in The Lancet, another diagnosis had initially been erroneously proposed. Even more so in the isolated health centers, it is probable that cases of AIDS have escaped the curiosity of clinicians during several years” (author translation).

    It should also be mentioned that extensive urbanization took place in the Congo during the last 40 years. Between 1957 and 1985, the urban population rose from <10% to 40% [8].

  84. jack lecou says

    Hmm. I think the phrase is “wild accusations”. And I don’t know what happened to the blockquote. Oh well.

  85. GerrardOfTitanServer says

    That all sounds like it’s been rather well covered long ago. As an aside, this conspiracy is pretty bonkers. Apparently, they can’t even decide on which continent the nefarious vaccines are supposed to have been made. The phrase “while accusations” comes to mind.

    It was a hypothesis. Hypotheses change. This changed once. Tom Curtis didn’t know about it when he published his article in The Rolling Stone, and Edward Hooper didn’t know about it until a little bit later.

    They back-calculate that the number of infected individuals already exceeded 10 in Léopoldville in 1952 ± 5 years, placing the introduction well before the first OPV vaccination.

    Gods-damn it. More circular reasoning. More dating based on the assumption of a single patient zero.

    The combination of rarity of infection, perhaps confined to individuals in rural areas, plus the lack of medical care in those areas would have allowed isolated illnesses and deaths to pass unnoticed. Moreover, the fact is that AIDS in the Congo went unnoticed for over 20 years (from the early 1960s to 1983), even as it was becoming more prevalent.

    It was noticed by certain doctors years before 1983. It was noticed by the community in other countries years before that, known as the “Slim”. Your source is wrong.

    The answer is clearly yes, and there are many arguments for this statement, assuming that HIV/AIDS was sporadic before that date.

    Key word – sporadic. How could it remain sporadic for the assumed 50 years without becoming pandemic? It explosively became a pandemic 50 years later, and they claim it simmered somehow for 50 years to remain below detection thresholds.This is implausible.

  86. Rob Grigjanis says

    Gerrard @88:

    Finally, I’m no expert, but it’s also my understanding that the HIV phylogenetic tree is quite unusual. It’s a starburst pattern. That’s highly unusual.

    There are papers going back 20 years which claim to debunk the supposed importance of the starburst pattern to the OPV hypothesis. I’m not an expert either, but the arguments seem reasonable to me. Have you read any? Here’s one; “Phylogeny and the origin of HIV-1”

    http://evolve.zoo.ox.ac.uk/Evolve/Oliver_Pybus_files/Phylogeny%26TheOriginOfHIV.pdf

  87. GerrardOfTitanServer says

    Rob
    Thanks. I read it, but I don’t see how it’s an explanation. They end with this:

    Our results indicate that the Congo andglobal phylogenies probably result from dif-ferent epidemiological histories. As manyCongo strains appear to be basal, we proposethat each global subtype is the result of thechance exportation of some Congo strains toother geographical regions, thus producing anapparent starburst. Such founder effects have been proposed to explain the phylogeneticallydistinct subtypes B and E of HIV-1 group M(ref. 2). The observation that many Congostrains fall basal to the global subtypes alsosuggests that previous phylogenetic analysishas underestimated the number of lineagesthat pre-date 1957–60, and hence underesti-mated the minimum number of cross-speciestransmissions necessary to reconcile the OPVhypothesis with phylogenetic data.In conclusion, the HIV-1 sequences fromthe Congo are evidence that the claim of theOPV theory1that it is “probably the onlyhypothesis of origin that can readily explainthe starburst phenomenon” is incorrect. Ourresults give us no reason to doubt that the lastcommon ancestor of HIV-1 group M waspresent in a human host.

    The first part is just a restatement of what I claimed: There’s a bunch of strains that appear to be equidistant from each other, e.g. starburst pattern.

    They do nothing to explain this highly unusual data except to propose an unsatisfactory ad-hoc explanation that involves a series of amazing coincidences (all of the separate subtypes spread to separate neighboring countries in the same year, and they didn’t spread to neighboring countries in the prior 50+ years before that). Supposing that all of the strains existed for so long without spread, only to all spread at exactly the same time 50 years later – that’s incredibly ad hoc. Too many coincidences without explanation. It’s implausible.

    They don’t mention the necessary minimum number of crossovers for the CHAT OPV hypothesis to be true, which I find deeply unsatisfying.

    Their conclusion sentence seems to me to be radically disconnected from everything that follows from before. I’m not sure that I get it. It seems like they’re saying “we can propose an unlikely ah hoc explanation that fits the data, and therefore because of reasons unexplained, our ad hoc explanation is as likely or more likely than the CHAT OPV hypothesis”. The whole point is that the starburst pattern is that it’s something very unusual which demands demands an explanation. These authors don’t give an explanation besides shrugging their shoulders and saying “it was chance”. That’s deeply unsatisfying.

    At least other authors try to point to certain social and cultural changes circa 1960 to explain how we go from A- zero spread to neighboring countries and near zero spread inside the country to B- to massive spread inside the country and to neighboring countries in a very short period of time. (I find these explanations to be deeply unsatisfying and also based on incorrect history of Africa AFAICT.) These authors didn’t even go that far.

    Did I miss anything?

  88. John Morales says

    “Did I miss anything?”

    This, apparently:

    This indicates that the structure of HIV-1 phylogenies is the result of epidemiological processes acting within human populations alone, and is not due to multiple cross-species transmission initiated by oral polio vaccination.

  89. GerrardOfTitanServer says

    John, but what is the basis of that conclusion? How did they reach that conclusion? I don’t get it.

  90. John Morales says

    Gerrard, could it possibly be that you’re no expert, but that they are?

  91. John Morales says

    Ahem, Gerrard. That’s the whole point. You can’t figure out how the experts have come to their conclusion, so you question it.

    Specifically, you ask me to explain the wherebys of their conclusion, to your satisfaction no less.

    (It’s not hard to see that you asking me is purely rhetorical.
    And not in a good way)

  92. jack lecou says

    Gods-damn it. More circular reasoning. More dating based on the assumption of a single patient zero.

    Ten, actually.

    But it doesn’t really matter — it’s just a transmission model. Obviously if you start with ten and run the model then at some point you have a hundred, and then ten thousand and then a million.

    And if you want to suppose that, say, 100,000 people were infected simultaneously to start*, then to the right of that point the curves should be exactly the same shape. You can just ignore everything to the left. (IRL, the geographic distribution of that 100,000 might be distinguishable, but that’s not covered by this model.)

    Now, given that, I’d agree that you can’t necessarily use that to work backward from the number of infections in 1990, say, and conclude that there were necessarily X number in 1950. Obviously if there are no data points that far back, then 0 in 1950 and a sudden jump to 1000 in 1959 could fit the data just as well. At least as long as f(1959)=1000 is consistent with the growth forward to f(1990)=Z or whatever.

    However.

    It does show how an explosive pandemic in 1980 can be perfectly consistent with a bare handful of cases in 1950 or earlier, given a moderately realistic model of how the disease spreads. Which makes this silly statement look like the innumeracy it is:

    Key word – sporadic. How could it remain sporadic for the assumed 50 years without becoming pandemic? It explosively became a pandemic 50 years later, and they claim it simmered somehow for 50 years to remain below detection thresholds.This is implausible.

    I’m really not sure why you think that’s so implausible. It is frankly just the way exponential(-ish) growth works. If you look at different parts of an exponential curve in isolation, the left side may very well look almost flat — “simmering sporadically for 50 years” — even as the right side is seemingly shooting up a cliff. Nevertheless, it’s all just one continuous curve.

    It was noticed by certain doctors years before 1983. It was noticed by the community in other countries years before that, known as the “Slim”. Your source is wrong.

    No, their characterization seems about right. Nobody was ringing any alarm bells in the 60s, certainly. And while there are individual case reports from those decades, I’ve seen no evidence from you or elsewhere that doctors were noticing it in any systematic way until the early 80s. I’m not sure when the public began taking notice of “Slim”, but if popular recognition preceded the doctors’, that’s hardly a resounding endorsement of the medical community’s acuity to the matter.

    So, let’s say “notice” is sometime in the mid to late 70s. Generously. That still means it’s going unnoticed — certainly not officially recognized as a disease — until essentially the point that growth is is reaching the knee on the exponential curve and starting to take off. That is, once again, really, really, reallllly bad evidence for your assertion that it would definitely have been noticed decades earlier if it was around, when the prevalence would have been far over to the left in the flat part of the curve. I’m just not sure why you think this argument is a winner.

    I’m actually a bit in the dark about how many infections were supposed to have resulted. Even if a half million people are inoculated with a straight up mad-scientist SIV culture, presumably that doesn’t mean you have anywhere near half a million HIV infections. I assume the actual successful crossover rate is still pretty low — might have to be to match the number of variants, and what’s known of their phylogenetic histories, assuming you can get that to match up at all.

    And then there’s the trypsinization issue — trypsin does indeed inactivate HIV. Even granting everything else in the theory, the number of doses that would actually have had viable SIV contamination might have been vanishingly small, if not zero. And then the SIV->HIV crossover probability would take its bite.

    If the highest you can pump this is, say, 5 or 10 people “successfully” infected by the vaccine in 1957, I’m not sure that matches observation. We have almost that many potential medically observed cases of full blown AIDS — in adults, even though it was children who received the vaccine — just a year or two later.

  93. GerrardOfTitanServer says

    And then there’s the trypsinization issue — trypsin does indeed inactivate HIV.

    There’s no firm evidence that trypsin was used in the local amplification of CHAT OPV in Congo. Note that most of the lab notebooks and other materials from CHAT OPV are lost. All we have are the testimony of the people directly involved, testimony in which they have remained uncertain about which kind of monkey was used, and sometimes contradicted themselves about what kind of monkey was used. The simplest explanation is that they’re lying and trypsin wasn’t used in the chimp cell cultures.

    We have almost that many potential medically observed cases of full blown AIDS — in adults, even though it was children who received the vaccine — just a year or two later.

    I don’t think we do. Could you be more specific please? Let’s go through them like Hooper does in The River. Note that we don’t have reliable HIV test results for any of them.

    Cases that probably weren’t HIV/AIDS:

    1- Sadayo Y., Montreal, died 1945. Negative PCR tests for HIV from samples.

    2- Alice S., Washington State, died 1964. No reliable HIV test. No obvious risk factors. Progression of the disesase was too rapid for HIV/AIDS.

    3- Ardouin Antonio, died 1959. Probably berylium poisoning from having to break and dispose many fluorescent light bulbs at his job.

    Cases that might have been HIV/AIDS.

    4- Dick G., Tennessee, died 1952. Speculative explanations include: HTLV-1 infection from overseas girlfriends while in the military.

    5- David Carr, aka the Manchester Sailor, died 1959. Postiive HIV test result was later shown to be likely the result of contamination. Never visted Africa while in the navy.

    6- George Y., Toronto, died 1959. Speculative explanations include: inhaled uranium dust poisoning on the job, HTLV-1 infection.

    7- Robert R., St. Louis, Missouri, who died in 1969. No reliable HIV test. No obvious risk factors. Unusual presentation for an HIV/AIDS victim. Speculative explanations include: cadmium poisoning from a well-documented army weapons test near where he lived in the black part of the city.

    Again, there are other causes of AIDS-symptoms besides HIV. They are incredibly rare, but one cannot confidently diagnose HIV/AIDS from mere symptoms to a high enough certainty for our purposes here because we know that there exists a background rate of such cases for all of human history.

  94. GerrardOfTitanServer says

    I’m hitting an auto-filter. Not sure why. Have to experiment to find out. Sorry.

    No, their characterization seems about right. Nobody was ringing any alarm bells in the 60s, certainly. And while there are individual case reports from those decades, I’ve seen no evidence from you or elsewhere that doctors were noticing it in any systematic way until the early 80s. I’m not sure when the public began taking notice of “Slim”, but if popular recognition preceded the doctors’, that’s hardly a resounding endorsement of the medical community’s acuity to the matter.

    See quotes at the end. Not sure if they meet your standard of proof.

    So, let’s say “notice” is sometime in the mid to late 70s. Generously. That still means it’s going unnoticed — certainly not officially recognized as a disease — until essentially the point that growth is is reaching the knee on the exponential curve and starting to take off. That is, once again, really, really, reallllly bad evidence for your assertion that it would definitely have been noticed decades earlier if it was around, when the prevalence would have been far over to the left in the flat part of the curve. I’m just not sure why you think this argument is a winner.

    See quotes at the end. Not sure if the quotes will be persuasive.

    Random quotes from “The River” which are relevant.

    “The River”, pg 164

    Furthermore, would ancient AIDS really have gone unrecognized and unre­marked? Although typical AIDS symptoms such as fever, TB, wasting, and pneumonia would not be expected to cause ripples of concern in a rural hospi­tal in the first half of the twentieth century, the same could surely not be said of rarer presentations, such as cryptococcal meningitis or esophageal candidia­sis.65 Experienced doctors of the caliber of Jack Davies in Uganda and Jean Sonnet in the Belgian Congo insist that such conditions were simply not seen prior to the 1960s.

    “The River”, pg 764 – 765

    In the course of following up on these cases, I came across the name of Jack Davies, who had headed the Pathology Department of Mulago Medical School in Kampala between the forties and sixties. I phoned him and, to my surprise, Dr. Davies promptly announced that he thought the first AIDS case in Uganda had appeared in 1960. I asked how he could be so precise, and he answered that he and his Mulago colleagues had been trying to establish a teaching collection of pathology slides, but after reviewing twenty thousand autopsies spread over seventeen years, had still not come across a case of Pneumocystis carinii pneu­monia. Then, in 1960, an instantly recognizable case of PCP had cropped up. Dr. Davies recalled that the patient had been a man, and that in addition to the pneumonia he had had dysentery or some other form of wasting disease; but he could recall no other details, such as age or ethnic group.
    […]
    There are, however, possible alternative explanations for the apparently low­ered immunity of these emigrants.
    […]
    Equally, however, it cannot be denied that something unusual may have been happening — and that some of these people may have been among the first to die of AIDS.

    “The River” pg 89

    For it was here, in early 1983, that an African form of AIDS was first recognized by an Africa-based physician — Dr. Anne Bayley.

    During the seventies and eighties, Dr. Bayley was professor of surgery at the University Teaching Hospital (UTH), the only public hospital in Lusaka. She clearly recalls the “Eureka moment”— the day when she realized that some­thing different was happening with the KS cases in her ward. “I had been seeing about eight to twelve cases every year since 1978 — a very steady level,” she explains. “And then one day — it was in the January of 1983 — I went into my ward to do a round, and I realized that there were nine cases of KS in there at once.” Many of these were of a very different, more aggressive type of KS, accompanied by swollen lymph nodes. “I realized that I was seeing a new man­ifestation of the disease. And I remember being frightened. I’d never seen this range of presentations before, and I knew this disease well. These people responded to chemotherapy, but then the disease recurred within two, three or four months.” Dr. Bayley also began to realize that the socioeconomic back­ground of the patients was changing, and that a different, wealthier, more edu­cated group appeared to be more susceptible to this new form of the disease.

    During the first five months of 1983, she gradually became persuaded that this new form was the same as the aggressive KS being seen in American gays. By the end of the year, she had seen ten of the old-style KS patients, all ten of whom were still alive and well, together with thirteen of the new-style KS patients — eight of whom had died.1 Absolute confirmation of causation came in 1985, when one of her 1983 patients returned to the hospital, and his blood was found to be HIV-positive.

    “The River” pg 38-39

    Dr. Margerete Bundschuh is a German missionary doctor in her seventies, who worked in the country for thirty-one years. Until 1980, she was based at Kagondo hospital, to the south of Bukoba in the middle of Kagera district, and during this period she saw no cases that — even in retrospect — were suggestive of AIDS.18 But at the start of 1981 she moved to the hospital at Mugana, situated fifteen miles northwest of Bukoba and a similar distance south of Lukunyu. She recalls that in June 1981 five women from one of the border villages “in the free-trade zone beside Lake Victoria” attended the hospital. All were suffering from anaer­obic ulcers, which had destroyed the anal sphincter and the whole perianal region. A man from the same area also visited at around this time; his penis was apparently “half rotted off.” After quite lengthy treatment, but without any clin­ical improvement, the patients returned home and were never seen again. Dr. Bundschuh thought that the cause was the virus Molluscum contagiosum, complicated by “serious immune-deficiency.”

    “The RiveR”, pg 33-34

    In the late afternoon, as the shadows lengthened beneath Kasensero’s single tall tree, one of the elders called a meeting, so that the villagers could tell us about the disease, which had first arrived there some four years earlier. Since that year of 1982, over a hundred people — both Kasensero residents and those who came down to the lake to fish, or smuggle, or sell their bodies — had succumbed to the new disease. These persons had died in a variety of nasty ways. The mouths and throats of some had filled with a strange, creamy paste that would not go away; others had been racked with coughs and fevers, had developed sores on face and body, or had been plagued with constant diarrhea.

    The one common factor seemed to be that nearly all had become thin and shrunken, like the wraiths and ghouls and nightwalkers that are a constant theme in Kiganda folklore. It was perhaps for this reason that the Baganda peoples of Kasensero and the surrounding district of Rakai (and, later on, the central part of Uganda around the capital, Kampala) readily identified the sick­ness as something unprecedented in their area — and as a single entity, rather than a syndrome of many different conditions.2 And since this was clearly a new disease, they chose a new name for it: a descriptive name, but also one that was sweet and rather sad. The Baganda love playing with words and, given the violence of their recent past, have developed an affinity for hidden meaning and double entendre. What is more, as a nation of shopkeepers, they have taken brand names and the other paraphernalia of capitalism to their hearts. And so, with a playful nod to the cut then popular in Western shirts and to the elfin figures then fashionable among Western women, they called this new dis­ease “Slim.”The s

  95. GerrardOfTitanServer says

    “The River”, pg 164

    One of the few documented examples we have of early HIV infection in a rural area came about as a result of the blood samples taken at the time of the Ebola epidemic of 1976 from Yambuku/Yandongi in northern Congo. Some 0.8 percent of blood samples subsequently tested positive for HIV-1 — and when a cross section of the pop­ulation was again tested in 1985, exactly the same percentage was infected.This, therefore, would appear to be a good example of a stable rural epi­demic of HIV-1. And yet these were certainly not invisible, or subclinical, infec­tions.68 Three of the five HIV-positive people detected in Yandongi in 1976 had already died of AIDS-like disease by 1986, and one of the other two was clearly immunocompromised and in decline. Yet only one of these four (the femme libre), had ever lived outside rural Equateur province — in Kinshasa — and it is hard to imagine that the other three were all infected as a result of contact (indirect or direct) with her.69 In other words, these three appear to have been living a typical rural lifestyle, and yet they too were vulnerable to AIDS. HIV was, it seems, already pathogenic in this rural setting in the mid-seventies, even if it failed to spread as dramatically as it was about to do in the more hedonis­tic urban environment.

    “The River”, pg 98

    In fact, there are certain even earlier cases of AIDS in people from the Congo — some clinically likely, and others serologically confirmed — all of which involve children. One such was the son of a Congolese government official. The boy, born in August 1974, began presenting with typical symptoms of AIDS five months later in Kinshasa. In 1978, the whole family (mother, father, and three children) moved to Stockholm, where the boy eventually died in September 1982, at the age of eight. Stored blood samples taken between 1978 and 1982 later tested HIV- positive,40 and other information subsequently released by one of his doctors makes it clear that this was almost certainly a case of perinatal infection. His two siblings, born in 1970 and 1972, both tested HIV-negative.

  96. GerrardOfTitanServer says

    “The River”, pg 164

    One of the few documented examples we have of early HIV infection in a rural area came about as a result of the blood samples taken at the time of the Ebola epidemic of 1976 from Yambuku/Yandongi in northern Congo. Some 0.8 percent of blood samples subsequently tested positive for HIV-1 — and when a cross section of the pop­ulation was again tested in 1985, exactly the same percentage was infected.This, therefore, would appear to be a good example of a stable rural epi­demic of HIV-1. And yet these were certainly not invisible, or subclinical, infec­tions.68 Three of the five HIV-positive people detected in Yandongi in 1976 had already died of AIDS-like disease by 1986, and one of the other two was clearly immunocompromised and in decline. Yet only one of these four (the femme libre), had ever lived outside rural Equateur province — in Kinshasa — and it is hard to imagine that the other three were all infected as a result of contact (indirect or direct) with her.69 In other words, these three appear to have been living a typical rural lifestyle, and yet they too were vulnerable to AIDS. HIV was, it seems, already pathogenic in this rural setting in the mid-seventies, even if it failed to spread as dramatically as it was about to do in the more hedonis­tic urban environment.

  97. GerrardOfTitanServer says

    “The River”, pg 98

    In fact, there are certain even earlier cases of AIDS in people from the Congo — some clinically likely, and others serologically confirmed — all of which involve children. One such was the son of a Congolese government official. The boy, born in August 1974, began presenting with typical symptoms of AIDS five months later in Kinshasa. In 1978, the whole family (mother, father, and three children) moved to Stockholm, where the boy eventually died in September 1982, at the age of eight. Stored blood samples taken between 1978 and 1982 later tested HIV-positive,40 and other information subsequently released by one of his doctors makes it clear that this was almost certainly a case of perinatal infection. His two siblings, born in 1970 and 1972, both tested HIV-negative.

  98. jack lecou says

    The simplest explanation is that they’re lying and trypsin wasn’t used in the chimp cell cultures

    That doesn’t sound simple at all. It sounds very much like special pleading. Trypsin is a dead common way to get cultures loose. Why wouldn’t they have used it?

    Let’s go through them like Hooper does in The River. Note that we don’t have reliable HIV test results for any of them.

    I mean, those, but then literally from your own quotes:
    Then, in 1960, an instantly recognizable case of PCP had cropped up. Dr. Davies recalled that the patient had been a man, and that in addition to the pneumonia he had had dysentery or some other form of wasting disease

    Dying of late stage AIDS in 1960. If so, that means the probable infection would be circa 1950, not ’57 or ’58. All of these hyper-accelerated progressions you need to make things work are stretching credulity. And once again an adult — how are all these adults getting children’s vaccines?

    Or there’s this woman in the excerpt I quoted above:

    A case of possible AIDS seen in Léopoldville in 1962 [55] is mentioned in The River, and an attempt is made to link it to CHAT vaccination in Lisala in 1958. However, the case history related in the book shows that the woman was already symptomatic in 1958.

    Symptomatic. In ’58(!)

    You’re trying to hold up a collapsing house of cards, man.

  99. GerrardOfTitanServer says

    One or two cases, in 1959, in the Congo, is not a disproof. In rare cases, HIV infection does proceed to AIDS symptoms in just a small number of years. Typical time in the US was 10 years, but IIRC typical time in Africa was 4 years. Maybe due to the higher virulence of the earliest strains, and maybe because of poorer typical health, nutrition, medical care, etc.

  100. jack lecou says

    in early 1983..recalls that in June 1981…that year of 1982
    I am rather…unsure what you think this shows.

    It certainly does not appear to show a bunch of physicians recognizing the pandemic before 1980.

    This, therefore, would appear to be a good example of a stable rural epi­demic of HIV-1. And yet these were certainly not invisible, or subclinical, infec­tions.

    Maybe this garbage is what’s confusing. The way they’re using “invisible” here seems to be implying that they think someone expects it to be synonymous with “asymptomatic” (i.e., subclinical).

    AFAIK, that’s not what anyone expects. All you need is that symptoms and deaths in these kind of rural populations were far less likely to be noticed or recorded. Which is eminently plausible, including for this very case, and only reinforced by the reams of accounts you’re conveniently providing, of doctors not noticing the pandemic until it was striking people, especially people in the cities, down in job lots.

  101. jack lecou says

    My sources suggest that the cell cultures were primitive Maitland-type cultures which were typically made without trypsin. More information here:

    Your source literally says the opposite of that.

  102. GerrardOfTitanServer says

    My sources suggest that the cell cultures were primitive Maitland-type cultures which were typically made without trypsin. More information here:

    Your source literally says the opposite of that.

    I meant Hooper suggests it, and this is the first non-Hooper source that I found. AFAICT, Maitland-style cell cultures were approved for polio vaccines at the time, and Maitland-style cell cultures were being performed in the Wistar lab in Leopoldville in Congo circa 1958 by their own admission. Not for vaccine amplification according to the words of Koprowski’s confederates, but for other experiments.

  103. jack lecou says

    One or two cases, in 1959, in the Congo, is not a disproof. In rare cases, HIV infection does proceed to AIDS symptoms in just a small number of years. Typical time in the US was 10 years, but IIRC typical time in Africa was 4 years. Maybe due to the higher virulence of the earliest strains, and maybe because of poorer typical health, nutrition, medical care, etc.

    I will happily grant you “a small number of years”. Nevertheless, I think someone becoming symptomatic in 1958, within the very same year they were supposedly vaccinated is rather straining credibility.

  104. jack lecou says

    AFAICT, Maitland-style cell cultures were approved for polio vaccines at the time, and Maitland-style cell cultures were being performed in the Wistar lab in Leopoldville in Congo circa 1958 by their own admission. Not for vaccine amplification according to the words of Koprowski’s confederates, but for other experiments.

    None of which actually addresses the correspondent’s point in your link, about the difficulty and lower yields with the kidney cultures.

    The “words of Koprowski’s confederates” make imminently practical and logical sense here. There’s only so much you can actually prove by just calling everyone liars.

  105. GerrardOfTitanServer says

    I’ll count it as weak evidence against. However, AFAIK, it wasn’t confirmed HIV/AIDS from later PCR testing, and so we don’t know for sure that it was HIV/AIDS. And if it was HIV/AIDS, it’s still plausible. Latency / incubation time can be as little as 1 year. I’m still trying to track down sources of the shortest confirmed incubation period.

    http://hivinsite.ucsf.edu/InSite?page=kb-03-01-04

    HIV disease is a continuum of progressive damage to the immune system from the time of infection to the manifestation of severe immunologic damage by opportunistic infections (OI), neoplasms, wasting, or low CD4 lymphocyte count that define AIDS. The time it takes to traverse this spectrum varies greatly, ranging from 1 year or less in some persons to a still unknown upper limit in others that has reached nearly 20 years in a few individuals.

    https://canfar.com/stages-of-hiv-infection/

    People can also progress through the various stages of HIV infection at different rates, with some folks so-termed “rapid progressors” seemingly developing to AIDS within perhaps 2 years.

  106. GerrardOfTitanServer says

    None of which actually addresses the correspondent’s point in your link, about the difficulty and lower yields with the kidney cultures.

    Again, Maitland-style cultures were an approved way of creating polio vaccine, and other people were doing it, and so the objection about yields is moot. We know that the lab had staff and equipment to do Maitland-style cultures, and so the other objection is moot.

  107. jack lecou says

    Again, Maitland-style cultures were an approved way of creating polio vaccine, and other people were doing it, and so the objection about yields is moot. We know that the lab had staff and equipment to do Maitland-style cultures, and so the other objection is moot.

    If I say, “making cookies with technique X is easier than technique Y, and you get more cookies” it is not a rebuttal in the slightest to say “but it’s possible to make cookies using technique Y, and you have the equipment for it”. You certainly won’t have proved that I’ve secretly been using technique Y this whole time.

    I’m not even sure how you can possibly think that.

  108. GerrardOfTitanServer says

    One creator of one polio vaccine, Glaxo, used Maitland-style cultures. This source even mentions how inefficient it is. Yet, this person did it.
    https://www.jstor.org/stable/3067035?seq=1#metadata_info_tab_contents

    Also
    https://journals.sagepub.com/doi/pdf/10.1177/003591575705001219

    The other method of bulk preparation of poliomyelitis viruses is the one introduced by the Connaught Laboratories in 1952 and is essentially a large-scale version of the Maitland technique whereby the tissue is chopped into pieces about 1 to 2 mm. in diameter which are allowed to float free in the nutrient medium. This method was the one employed for the preparation of the virus in 1953 which was later processed into vaccine in the U.S.A. for the Fiel dTrial in 1954 (Farrell et al., 1955) and is the one we employ at Sefton Park. Super-ficially, it is a much less elegant technique than the trypsinized cell method and the titres of the virus pools produced are slightly lower. However, in practice, it is a most trouble-free operation to manage, and as the procedures carried out are independent of any demonstration of cell growth – which indeed may not occur – considerable latitude is available in the timing of the inoculation and harvest stages.

    Thus, your argument “they (probably) didn’t use Maitland cultures because its inefficient” is a bad argument. Clearly others did use Maitland cultures to create polio vaccine, and they could have done so as well in the Wistar lab in Congo.

  109. GerrardOfTitanServer says

    https://www2.health.vic.gov.au/public-health/infectious-diseases/disease-information-advice/hiv-and-aids

    The interval from HIV infection to the diagnosis of AIDS ranges from about 9 months to 20 years or longer, with a median of 12 years. There is a group of people with a more rapid onset of disease who develop AIDS within 3–5 years of infection, and another smaller group who do not seem to progress to AIDS.

    9 months is an oddly specific number. There must be some case study which I cannot find with my weak google-scholar kung-fu. So, less than 1 year from infection to AIDS symptoms is not unprecedented.

  110. says

    Just a couple of things so people aren’t fooled by Gerrard’s dishonesty.

    It was standard practice to amplify the vaccines locally.

    Citation needed. (If it is just the conspiracy theory author again don’t bother)

    Nurses working there testify on camera that they sacrificed hundreds of chimps and got their kidneys.

    Again citation needed. And note, unless they specifically say they were harvesting kidneys for polio virus amplification, this is a non-sequitur.

    There is evidence of hundreds of chimps being shipped to the lab in Congo and being killed. There is no reason for such an extremely high number of chimps being sent to a lab in the middle of nowhere and killed unless they were being used to amplify the vaccine.

    Argument from personal incredulity, which seems to be a mainstay for conspiracy theorist. There is of course no actual evidence that the chimp autopsies had any connection to the polio vaccines.

    Here. Let me say it again for your benefit. These papers are assuming the cut-hunter hypothesis to be true as a starting assumption for their dating methods. In other words, they’re assuming that there was a single viral crossover from chimps to humans. In other words, they’re excluding the possibility a priori of a punctuated event, of multiple crossovers at about the same time, which is plausible if not likely on the CHAT OPV hypothesis. In other words, using these papers to debunk the CHAT OPV HIV/AIDS hypothesis is simply an exercise in circular reasoning.

    And that’s before we get into the fatal methodological problems of dating by constant mutation rate for a virus that changes primarily by recombination.

    Claiming something repeatedly doesn’t make it so. You clearly haven’t read the research/don’t understand it. But I’ll let you have your chance. Show your work. Show where the work done in those papers relies on a particular transmission to reach their conclusions regarding origin timing. (And just to head of an obvious dishonesty, citing or mentioning the standard hypothesis which could be found unsupported by a work doesn’t count. ) Show how using the observed mutation rate (which includes recombination) of HIV-1 is wrong when using its rate in calculations.

    I think others have done a fairly good job of pointing out other dishonesty.

  111. GerrardOfTitanServer says

    Bingo.
    https://www.scielo.br/j/bjid/a/RqJJRbGfzXX43v9fgzdsgjL/?lang=en

    Acute HIV infection is rarely recognized as the signs and symptoms are normally unspecific and can persist for days or weeks. The normal HIV course is characterized by a progressive loss of CD4+ cells, which normally leads to severe immunodeficiency after a variable time interval. The mean time from initial infection to development of clinical AIDS is approximately 8-10 years, but it is variable among individuals and depends on a complex interaction between virus and host. Here we describe an extraordinary case of a man who developed Pneumocisits jiroveci pneumonia within one month after sexual exposure to HIV-1, and then presented with 3 consecutive CD4 counts bellow 200 cells/mm³ within 3 months, with no other opportunistic disease. Although antiretroviral therapy (AZT+3TC+ATZ/r) was started, with full adherence of the patient, and genotyping indicating no primary antiretroviral resistance mutations, he required more than six months to have a CD4 restoration to levels above 200 cells/mm³ and 10 months to HIV-RNA to become undetectable.

  112. GerrardOfTitanServer says

    Citation needed. (If it is just the conspiracy theory author again don’t bother)

    This is bordering on the absurd. Are criminal conspiracies among 5 business confederates suddenly impossible if they’re virologists? Because that seems to be the implication that you’re making. Calling him a conspiracy theorist is just a baseless ad hom, poisoning the well fallacy.

    Again citation needed. And note, unless they specifically say they were harvesting kidneys for polio virus amplification, this is a non-sequitur.

    No, it’s not. It’s not non-sequitir. It’s quite relevant.

    Show your work. Show where the work done in those papers relies on a particular transmission to reach their conclusions regarding origin timing.

    Have you tried reading the papers? They’re all about calculated the date of the recent common ancestor (MRCA), and then proclaiming that this date precedes 1957, and therefore HIV existed in humans before 1957. The term “most recent common ancestor (MCRA)” is by definition a single “organism” (or virus). The CHAT OPV hypothesis allows for, and even suggests, that the MCRA was inside of a chimp and not inside of a human, aka there were multiple concurrent crossovers from chimp to human which happened after the MCRA.

    Show how using the observed mutation rate (which includes recombination) of HIV-1 is wrong when using its rate in calculations.

    Uh… what? Mutation does not include recombination. In the context of molecular clock dating, they are different non-overlapping things. In some of the dating papers, they even explain how they have identified recombinant sequences and excluded them from the analysis because recombination is not mutation. Do you know what these words even mean in this context of molecular clock dating? I’m thinking that you don’t.

  113. GerrardOfTitanServer says

    Sources:
    https://retrovirology.biomedcentral.com/articles/10.1186/s12977-016-0269-6

    There are several factors preventing complete adherence to clock-like HIV-1 evolution. Recombination can alter coalescing patterns and thereby perturb clock-like diversification [46].

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470933/pdf/15280223.pdf

    Recombination is a frequent event in the evolution of HIV (Robertsonet al.1995), giving rise to a multitude of mosaic genomes, some of which are significant in the pandemic and termed “circulating recombinant forms” (Robertsonet al. 2000). Coestimation of recombination rates, varying population sizes, substitution rates, and complex substitution models within a coalescent framework is expected to be technically challenging and no algorithms are currently available for this task. Previous coalescent analyses of HIV epidemic history have therefore assumed no recombination within the genome fragment under investigation. Frequent recombination will result in different phylogenies along the HIV genome and, at its most extreme, will lead to a total loss of linkage between genes. Worobey(2001) showed that if a single tree is estimated from recombining sequences then estimates of rate heterogeneity among sites are biased upward and the terminal tree branches are lengthened, resulting in a possible overestimation of the TMRCA and a possible demographic bias toward exponential growth. More detailed simulations by Schierup and Forsberg(2003) have confirmed this effect. The impact of these effects on demographic estimates has yet to be quantified. Furthermore recombination — even at small levels — leads to a rejection of themolecular clock (Schierup and Hein 2000b).

    https://academic.oup.com/ve/article/5/2/vez036/5561482

    We compiled a data set of 465 HIV-1 group M genomes, including 104A, 82B, 93C, 63D, 45F, 60G, 9H, 7J, and two K genomes. In Supplementary Data, we detail how the data set was compiled on a subtype by subtype basis. This generally involved selecting a subset of genomes available on GenBank, merging data sets from previously published studies or a combination of both, followed by a filtering step (removing multiple genomes per patient, duplicates, unusually divergent genomes, cultured viruses, and outliers in a root-to-tip divergence analysis) and recombination screening.

    For HIV-1 group M analyses, we generally exclude subtypes G, H, J, and K because of the possible confounding effect of recombination (subtype G) (Abecasis et al. 2007; Lemey et al. 2009), and the low number of representative genomes (subtype H, J, and K).

  114. jack lecou says

    Thus, your argument “they (probably) didn’t use Maitland cultures because its inefficient” is a bad argument. Clearly others did use Maitland cultures to create polio vaccine, and they could have done so as well in the Wistar lab in Congo.

    That’s not the argument.

    The argument is, “They say they used trypsination. And it is known to be easier and more efficient.”

    We might have reason for a little bit of disbelief if the claim was the reverse — that they said they used Maitland cultures. “Why wouldn’t you have used trypsin?” we could object, “It’s easier and more efficient.” And they might feel obligated to provide at least a token justification.

    But since they were already using the more effective process for the job, there’s no reason to doubt their word just because others were using a less efficient process. That’s not how anything works.

    Also:
    1) Citation needed on the cultivation being done in Congo. IIRC, that’s a purely unsupported accusation. The vaccine production was in Philadelphia and Belgium.
    2) It’s also not just the trypsin. The various washing steps, filtration, etc., virtually the entire protocol, is reportedly quite hostile to any putative lentivirus hitchhikers. The Lancet letter you linked has a breakdown of the likely attrition through the various steps, most of which would still be factors even in a Maitland process (which might conceivably make its own contributions). And that’s on top of the fact that kidneys and kidney cells are known to be bad hosts for lentiviruses in the first place.

  115. GerrardOfTitanServer says

    The argument is, “They say they used trypsination. And it is known to be easier and more efficient.”

    Those are two arguments. The second is moot because other people chose the other method because they found it to be easier in spite of being less efficient. Again, see my sources up-page in post 118. Only the first argument has merit, which is basically saying “we should trust them”. I don’t.

    1) Citation needed on the cultivation being done in Congo. IIRC, that’s a purely unsupported accusation. The vaccine production was in Philadelphia and Belgium.

    You’re confusing several claims. One – Paul Osterrieth made cell cultures in the lab in Leopoldville. Two – these cell cultures were of chimp cells from locally sacrificed chimps. Three – these cell cultures were used to amplify the CHAT OPV vaccine on site. Claim one is admitted by Paul Osterrieth and contained in lab reports.
    https://documents.uow.edu.au/~bmartin/dissent/documents/AIDS/LRBletters03.html

    3. From Stanley Plotkin

    The 1958 report of the laboratory in which Paul Osterrieth worked recounts that cell cultures were achieved from baboon kidneys.

    So, there were cell cultures going on.

    Admitted by all, there were also the sacrifice of at least circa 50 chimps for medical experiments in the lab in Leopoldville. Koprowski et al say that these sacrifices were for reasons other than vaccine amplification and were for other medical experiments. Hooper claims to have evidence of IIRC more than 200 chimps being shipped there and sacrificed.

    Local amplification on site was a common practice by other OPV vaccine creators at the time. It would be odd if Koprowski hadn’t done it.

    It’s also not just the trypsin. The various washing steps, filtration, etc., virtually the entire protocol, is reportedly quite hostile to any putative lentivirus hitchhikers. The Lancet letter you linked has a breakdown of the likely attrition through the various steps, most of which would still be factors even in a Maitland process (which might conceivably make its own contributions).

    Let me remind you that SV-40 is a thing that happened with another vaccine. We know that monkey viruses can cross over in polio vaccines because they did. SV-40 did happen. Thankfully it appears to not be harmful to humans (or at most minimally harmful). The question is whether it happened again with SIV.

    You’re also assuming that these pioneers with zero oversight, on a budget and a race with other OPV developers, followed every safety step, while experimenting on borderline-forced and sometimes actually forced colonial black population. In this context, it’s far from a given for me that they followed all of the normal safety steps. They probably skipped some in the interests of saving time to be first to make the money and fame.

    And that’s on top of the fact that kidneys and kidney cells are known to be bad hosts for lentiviruses in the first place.

    Don’t care enough to look for a source right now unless you demand it, but I believe that this is out of date news, and HIV is pretty happy to grow there. Forget why. Was it a high white blood cell count in these organs? Don’t remember, but I recall reading something that says that this common wisdom is wrong.

  116. GerrardOfTitanServer says

    Ah, from a source you won’t like:
    http://www.aidsorigins.com/the-origins-of-the-aids-pandemic/

    To cast more light on the question of whether SIVs would survive through to the final vaccine, let me quote an American virologist who has worked on HIV/AIDS for almost 30 years, from an email written to me in 2003: “An exploded kidney contains macrophages. HIV and SIV reside in macrophages, can be produced by macrophages, and can replicate in macrophages…The plausibility of whether OPV could have been the source [of AIDS] boils down to whether chimps were used on site [ie in Africa] for the production of [batches] used in the human testing.”

  117. GerrardOfTitanServer says

    From a source that you might like:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579771/

    Abstract
    Objectives

    HIV-1 can infect and persist in different organs and tissues, resulting in the generation of multiple viral compartments and reservoirs. Increasing evidence supports the kidney as such a reservoir. Previous work demonstrated that HIV-1 infected CD4+ T-cells transfer virus to renal tubule epithelial (RTE) cells through cell-to-cell contact. In addition to CD4+ T cells, macrophages represent the other major target of HIV-1. Renal macrophages induce and regulate inflammatory responses and are critical to homeostatic regulation of the kidney environment. Combined with their ability to harbour virus, macrophages may also play an important role in the spread of HIV-1 infection in the kidney.

  118. jack lecou says

    Evidence for a recombinant origin of HIV-1 Group M from genomic variation:

    We found evidence of substantial variation in estimated root dates among windows, with an estimated mean time to the most recent common ancestor of 1922. Estimates were significantly autocorrelated, which was more consistent with an early recombination event than with stochastic error variation in phylogenetic reconstruction and dating analyses. A piecewise regression analysis supported the existence of at least one recombination breakpoint in the HIV-1/M genome with interval-specific means around 1929 and 1913, respectively.

    Now, I’m not entirely confident that I’m truly grokking more than every other word or so there, but they seem to be saying that they’re modeling tMCRA (at least for group M), comprehensive of recombination events, and still getting estimates in roughly the same decade that a more “naive” molecular clock does.

    It sounds like further work on recombination and HIV sequencing will be very interesting, and provide insights into the early years of its evolution. It doesn’t sound like we should be expecting the actual dates for those ‘early years’ to be changing that much though.

  119. jack lecou says

    Those are two arguments.

    No. They’re the same thing. The reason someone might be using one method over another is absolutely integral to evaluating the plausibility of a claim that they were doing so. Splitting it apart just breaks down to nonsense.

    Again, look at the cookie analogy. This is just common sense.

  120. jack lecou says

    Let me remind you that SV-40 is a thing that happened with another vaccine.

    SV-40 is a polyomavirus. What the heck would that have to do with arguments about the protocol’s selectivity against a lentivirus? They’re not even in the same viral realm for Pete’s sake.

    Are they all just “monkey viruses” to you?

  121. jack lecou says

    Ah, from a source you won’t like…From a source that you might like…

    Yes. Macrophages. Which are, notably, a kind of cell that is not a kidney cell. Even when they happen to be in or around kidneys. But its kidney cells being the thing the thing the polio vaccine was cultured in.

    The OPV contamination story relies substantially on the hope that a sufficient number of residual macrophages will be collected together with the kidney cells proper, and subsequently manage to hitchhike along through the entire process. This is, as the sources have been saying, dubious.

  122. GerrardOfTitanServer says

    I’m not an expert, and I might be wrong, but I think the tl;dr of molecular clock dating is neutral drift.
    https://en.wikipedia.org/wiki/Neutral_theory_of_molecular_evolution

    A lot / most of the genome of many / most animals is junk DNA. I don’t know if this is true for viruses and HIV in particular, but work with me.

    Because these parts of the genome are non-functional, changes to them are not under selection pressure. Therefore, there is random genetic drift in these selections. By further assuming a simple constant rate of one-letter changes (“mutations” in this context), one can easily calculate a prediction for the amount of time to the most recent common ancestor for the two samples. Then, I’m sure one can do fancy things, like try to account for varying mutation rates.

    However, recombination is entirely separate sort of beast from random “letter” changes in the genome. It’s inserting, removing, and swapping large sections of “letters” from the genome. Thus, one should see how even one recombination event would utterly destroy a simple naive molecular clock dating procedure. So, some other authors of other papers tried to identify and remove recombinant strands and then assume there are none remaining to do their dating. I’m unaware of fancier techniques which might exist to try to deal with recombination, but it looks like this paper might be such a thing(?).

    From your source:

    https://academic.oup.com/ve/article/5/1/vey039/5298912

    In practice, these ‘dated-tip’ analyses of HIV-1/M diversity often rely on a number of assumptions including an absence of recombination, such that the entire span of the multiple sequence alignment (MSA) can be related through a single phylogeny (Korber et al. 2000; Worobey et al. 2008; Faria et al. 2014). Previous studies have shown that recombination can skew estimates of the molecular clock (Schierup and Hein 2000) and thereby estimates of times to common ancestors. For example, the transfer of divergent sequence by recombination from another subtype could inflate molecular clock estimates within the affected interval of the genome.

    And honestly I don’t understand half of the paper. It is saying that much of the earlier work is flawed because they basically assume no recombination or that they’ve accounted for it, but this paper says that it’s likely that there was a major recombination event early on in the evolution of HIV-1. I also note the given graph shows a wide variety of tMCRAs (time to most recent common ancestor), with quite a wide distribution depending on the region of the genome, with many regions of the genome closer to 1960, but I can’t grok enough of the paper on the first few readthroughs to really understand what that means.

    It does seem to validate most of what I was saying about the unreliability of earlier dating papers because they pretended that their samples didn’t have recombination.

  123. GerrardOfTitanServer says

    Again, look at the cookie analogy. This is just common sense.

    Again, I’m operating under the assumption that they’re lying to cover their accidental insertion of HIV into the human population. This is a competing explanation for what they’re saying. You’re still operating under the assumption that they’re being truthful, and I’m not.

    The OPV contamination story relies substantially on the hope that a sufficient number of residual macrophages will be collected together with the kidney cells proper, and subsequently manage to hitchhike along through the entire process. This is, as the sources have been saying, dubious.

    You did see this source, right?
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579771/

  124. jack lecou says

    So, there were cell cultures going on.

    I didn’t say cell cultures. I said vaccine production. Paul Osterrieth:

    At my return from the U.S.A., I attempted to set up a cell culture laboratory in Stanleyville. It was difficult to do so because of the lack of the adequate equipment and material. As I recall, several months passed before I was able to succeed in the cultivation of HeLa cells and of kidney cell cultures from baboons. Aside from the limited success with baboon kidney cell culture I also tried to start cell cultures from the kidney of other species of small monkeys. Trypsin was uniformly used to disperse the cells from tissue…. However, at no time did I ever attempt to make cell culture from chimpanzee tissues. In addition, I wish to state categorically that no poliovaccine was ever produced or could have been produced in Stanleyville, since the facilities were totally inadequate for a production or control of poliovaccine.

    You can’t just arbitrarily pick and choose which bits of testimony are most convenient to your narrative. Nor do you get to inveigle your way from “started a few cell cultures with great difficulty” to “produced hundreds of thousands of vacccine doses”.

  125. GerrardOfTitanServer says

    More fun! They were preparing chimp cell cultures of a sort at the lab in Congo.
    https://web.archive.org/web/20170518092713/http://www.bmartin.cc/dissent/documents/AIDS/Hooper03/Hooper03.pdf

    By good fortune, we happen to have a precise description of how a non-trypsinisedtissue culture was prepared in Stanleyville. This features in an internal reportpublished by the U.S. Armed Forces Epidemiology Board (AFEB) in 1959.53 TheAFEB report concerns the research into hepatitis in chimpanzees carried out by aPhiladelphia virologist, Fritz Deinhardt, who arrived in Stanleyville on February 1st,541958, and stayed until the end of April.55 He apparently collaborated with bothGhislain Courtois and Paul Osterrieth (in the microbiology and virology departmentsof the new laboratories), and he spent a lot of time at Lindi camp.

    In order to continue his hepatitis research in vitro after he had returned to the US, DrDeinhardt decided to transport chimpanzee cells back to Philadelphia. This wasfacilitated by the fact that, as explained in the AFEB report, there was already anexisting sacrifice programme which he was able to plug into.

    The passage in question reads: “Several chimpanzees used for poliomyelitis studies atthe Lindi camp had to be sacrificed at intervals. The doomed animals were bled oneweek prior to sacrifice, and the serum separated. The kidneys were removed underaseptic precautions, and transported to the laboratory in containers filled withHanks’ solution. They were then minced and to the washed pieces was added 5%isologous serum in Hanks’ solution. These preparations were shipped in an insulatedbox without refrigeration to Philadelphia, where they arrived within 3 to 5 days. Inspite of the long sojourn the tissue was viable and 3 of 4 specimens yielded, aftertrypsinisation, excellent cultures…. None of the cultures revealed evidence of foamyagents or other ECCO viruses.”
    […]
    In his article published in the Royal Society proceedings, Dr Osterrieth refers to thisepisode as follows: “It is true that six minced chimpanzee kidneys were sent to theWistar Institute at the request of Fritz Deinhardt, who came to Stanleyville to 22experiment with hepatitis infection of chimpanzees. Although I do not rememberexactly when that was done, no cultures were retained in Stanleyville.”57
    […]
    The second revealing aspect of Dr Osterrieth’s Royal Society statement is the keydetail that “cultures” were prepared from chimpanzee kidneys in Stanleyville (even ifhe goes on to say that no cultures were retained there).Osterrieth’s description of the minced chimp kidney preparations as “cultures” ishighly significant, for it reveals that he is referring to Maitland-type cell cultures,rather than trypsinised monolayer cultures. Maitland-type cultures were simple tomake, even in the fifties: the process required mixing together some minced-upkidneys, some serum and some growth medium, and then adding a few drops ofantibiotics. With Osterrieth’s new testimony, it becomes clear that Maitland-type
    23cultures were initially made from the chimp kidney cells, chimp sera and Hanks’solution in Stanleyville, and that later at least six shipments of these cultures wereforwarded to Philadelphia, and were treated on arrival with trypsin, to produce“excellent” trypsinised monolayer cultures for Deinhardt’s hepatitis work.61

    So, they had chimp cell cultures of the correct type in the lab in Congo. Hooper also claims evidence of hundreds of chimps shipped there and killed. And again, you’re calling me a conspiracy theorist for saying that on the basis of other evidence, I conclude that they’re lying, and conclude that they used the chimp cell cultures to amplify the CHAT OPV vaccine locally.

  126. jack lecou says

    This is a competing explanation for what they’re saying. You’re still operating under the assumption that they’re being truthful, and I’m not.

    Rather, you’re operating under the assumption that they are not truthful, and working backwords from there.

    Your argument is essentially that using trypsin would be convenient for their story. But their story is a lie. So using trypsin must be a lie. That kind of logic renders your entire argument conspiratorial and unfalsifiable.

    They actually had good reason to be using trypsin. It’s not just convenient to their story, it was convenient to the whole process of polio vaccine production. It makes perfect sense, independently of whether anyone is lying, and the only reason to reject the claim is that it’s inconvenient to your narrative.

    You did see this source, right?
    Yes:

    Once infected, RTE cells can in turn mediate infection of monocytes and T cells, supporting a ‘ping-pong’ infection model between immune cells and epithelial cells that sustains HIV-1 infection within the kidney.

    Sustained infection relies on a complete kidney environment, with the presence of immune cells, not just kidney cells.

  127. GerrardOfTitanServer says

    More fun. If I cared enough right now, I would validate every source here, but thus far I trust Hooper, and I won’t do it tonight. When they delivered CHAT OPV vaccine to other countries, they amplified it locally. It would be rather odd if they didn’t do the same in Congo.

    https://web.archive.org/web/20170518092713/http://www.bmartin.cc/dissent/documents/AIDS/Hooper03/Hooper03.pdf

    These papers (combined with certain comments by Dr Koprowski) revealed thesurprising and important information that during this period it was common practicefor live polio vaccines to be passaged again in the country which hosted the trials.105

    I looked, for instance, at the papers describing Koprowski’s major field-trial, whichinvolved feeding CHAT to more than seven million children in Poland, starting inJune 1959. Papers written by Koprowski’s Polish collaborators made no mention oflocal amplification of the vaccine. However, they revealed that CHAT must have beenpassaged again in a locally-prepared tissue culture before it was administered.106This practice both amplified the quantity of vaccine, and potentially boosted its titre,which might otherwise have fallen during the long sea voyage to Poland, for evenfrozen vaccine loses strength quite quickly after it leaves the original lab.107Subsequent amplification in the recipient lab meant that less vaccine had to be sentoverseas, but that – after dilution of the amplified vaccine to a suitably immunogeniclevel – more persons could be vaccinated. Local amplification thus made a lot ofsense.

    It is not known which substrate was used for amplification in Poland, but the kidneysof rhesus or cynomolgus macaques from Asia seem very probable. The cells of thesetwo species were then being used to make polio vaccines throughout Europe, and thePolish authors report that these same two species were used for safety testing theKoprowski vaccines in Poland.

    It is known that CHAT vaccine was also amplified in Sweden in 1960-1962, usingcynomolgus cells as a substrate, because a 1966 article reported this fact.108 And theevidence strongly suggests that the same thing happened to the CHAT that was fed toapproximately 1.7 million children in Switzerland and Croatia during the sameperiod.109

    This local amplification of the vaccine virus is not mentioned in any of the earlyarticles about the Koprowski field-trials. In fact, the first literature reference I havemanaged to find to local preparation of a Koprowski vaccine comes from a Yugoslavjournal published in 1964.110

    By contrast, the several articles which describe the large-scale CHAT trials of the latefifties allude only to “dilution” of the vaccine virus – or else hide behind an impreciseuse of language. (The possible reasons for this apparent coyness on the part ofKoprowski and his collaborators will be discussed below.)

  128. GerrardOfTitanServer says

    jack
    I’m comparing two hypotheses for their plausibility like a good little Bayesian. When evaluating the hypothesis that they’re lying, assume that they’re lying, and try to figure out a probability that they would lie. When evaluating the hypothesis that they’re telling the truth, then assume that they’re telling the truth, and figure out the probability that they would tell the truth.

    If the chimp cell culture vaccine amplification hypothesis is true – if that’s really what they did, it is highly likely that they would lie about it afterwards. A few business partners in a highly competitive field with lots of personal legal and financial liability, as well as ego and pride on the line, would easily lie about past misdeeds.

    It’s quite plausible that they used chimp cell culture because it was cheap and easily available, and they kept it a secret for economic competitive advantage, and afterwards they realized that they fucked up, and so they destroyed any paperwork and lied about it. No one claim here is outrageous or extraordinary. All of these claims are mundane and plausible.

    Sustained infection relies on a complete kidney environment, with the presence of immune cells, not just kidney cells.

    I’m an idiot. What’s your point? Plenty of SIV would already be in the kidneys when harvested from the sacrificed chimps, and macrophages would be left over to allow for more SIV reproduction. Combined with Maitland-style cultures, based on what I’ve read, it’s quite reasonable that SIV survived into the final vaccine.

  129. jack lecou says

    So, they had chimp cell cultures of the correct type in the lab in Congo. Hooper also claims evidence of hundreds of chimps shipped there and killed. And again, you’re calling me a conspiracy theorist for saying that on the basis of other evidence, I conclude that they’re lying, and conclude that they used the chimp cell cultures to amplify the CHAT OPV vaccine locally.

    Yes. That presentation is wildly conspiratorial. It looks like hinges on a tendentious over-interpretation of Osterrieth’s use of the word “culture”, in a way that’s frankly bizarre.

    The entire process is described exactly and transparently: some kidneys were extracted, chopped up, preserved in a salt solution, and shipped to the states. Where the recipient proceeded to immediately convert the product to a trypsinated culture.

    But, oops, Osterrieth used the word ‘culture’ in an offhand way. All bets are off. Now an entirely different process is inferred from whole cloth. What if instead of shipping the pieces to the US, they had added some serum, growth medium, and antibiotics and made a Maitland culture.

    They could have done that, right? Well, sure. They could also have taken the pieces and trypsinated them like Deinhardt was doing back in the states. Then they would have had “excellent” trypsinated cultures. Or they could have extracted some chimp livers instead, and then fried them up and served them with some fava beans and a nice chianti.

    This isn’t about what they could have done though. It’s about what they did. And according to Osterreiths testimony, they didn’t.

  130. GerrardOfTitanServer says

    And according to Osterreiths testimony, they didn’t.

    “Judge, I didn’t accidentally cause the deaths of millions of people worldwide!”
    “What’s your evidence?”
    “Because I say I didn’t do it.”

    The personal testimony of anyone involved in a culpable way is practically worthless in this matter, except to the extent that he might contradict himself or his fellow accused conspirators.

    If the only thing standing in the way of the OPV hypothesis is that half a dozen business partners lied to avoid public accountability for the worst public health disaster of mankind, I’m going with the OPV hypothesis every day of the week.

    Why are you valuing eye witness testimony so highly? Why are you valuing the eye witness testimony of the accused so highly? It makes no sense to me.

  131. GerrardOfTitanServer says

    Jack
    What’s your point? That conspiracies of a few business partners to avoid legal liability never happen? Or that adding the name “scientist” magically makes a human into an infallible human being who can never lie? You say that I’m being ridiculous? You’re being ridiculous for conflating conspiracy theories of millions of people without strong evidence, to a conspiracy theory of like 5 people with strong circumstantial evidence. Conspiracy theories are real. They happen. They definitely happen in order to avoid legal liability for past actions. Conspiracies of 5 business partners is far from extraordinary. It’s mundane. It happens all the time.

  132. jack lecou says

    I’m comparing two hypotheses for their plausibility like a good little Bayesian. When evaluating the hypothesis that they’re lying, assume that they’re lying, and try to figure out a probability that they would lie. When evaluating the hypothesis that they’re telling the truth, then assume that they’re telling the truth, and figure out the probability that they would tell the truth.

    Pretty sure that’s not Bayes. P(A|A) is nonsense.

    Maybe you mean the probability that they’d lie given that they caused AIDS, or the probability that they’d be telling the truth given that they didn’t. But that’s exactly what I’m saying: both of those are essentially unfalsifiable. You can write off everything contradictory to your narrative as “well, they would say that, wouldn’t they”. The concept of innocent until proven guilty also applies: if you truly have no independent documentary evidence that can contradict their testimony, you don’t have anything. An assumption that they’re lying isn’t an indictment.

    But there’s plenty of inferences we can make outside of the testimony. Take this trypsination thing. Right there in front of you, you have the account of experiments by a researcher worker on other stuff, Deinhardt, with no reason to cover up involvement in any horrific infection accident. And what is he doing? He’s casually treating his kidney cell culture with trypsin, like it’s the sensible thing to do or something.

    There’s plenty of other methodological stuff that’s more or less self-confirming. What about the size of the chimps? It’s stated in there that they were small — almost entirely made up of pre-sexual juveniles, because bigger chimps were too dangerous. That would mean the rate of SIV infection among them would also be quite low, even entirely negligible. Is that a lie? Did they actually use big, mean chimps because pre-sexual juveniles would be too convenient to the narrative?

  133. jack lecou says

    “Judge, I didn’t accidentally cause the deaths of millions of people worldwide!”
    “What’s your evidence?”
    “Because I say I didn’t do it.”

    Umm, in the US legal system, the next thing the judge would say, unless a competent prosecutor interjects in here with some kind of case based on concrete facts, would be “good enough. case dismissed.”

    You need actual evidence. “They could be lying” is not that.

  134. jack lecou says

    “GerrardOfTitanServer is the Zodiac Killer”
    “No I’m not”
    “Well, you would say that wouldn’t you. Look, If the only thing standing in the way of the Gerrard-is-the-zodiac-killer hypothesis is that he lied to avoid public accountability for the a nasty series of murders, I’m going with the Gerrard-is-the-zodiac-killer hypothesis every day of the week.”

  135. jack lecou says

    A few business partners in a highly competitive field with lots of personal legal and financial liability, as well as ego and pride on the line, would easily lie about past misdeeds.

    It’s a good deal more than just the core business partners, whoever it is you’re looping into that definition. Table 1 in the Gellin et al paper lists 17 people alone, all testifying to the absence of any use of chimp cultures. Another two are listed in the nearby text. Some of those (Koprowski, Osterreith) are presumably on your list of core conspirators, but some of them are just technicians or grad students, long moved on, who surely would face any personal liability in the matter.

    And that’s just people still alive circa 2001. There were presumably even more potential whistle-blowers in the decades previous. You really do have to be supposing a pretty big conspiracy.

  136. says

    GerrardOfTitanServer:

    The problem here is that you want to dismiss this by labeling it as a conspiracy theory, but it’s not a traditional conspiracy theory. We don’t need thousands or millions of conspirators to explain this. We need like 5, and conspiracies of five people happen all the time.

    Hm. I’m skeptical that such a conspiracy could have been maintained in this field for decades. Even if you limit it to this core handful of people, it would be surprising not to find deliberate or inadvertent admissions in communications to family, friends, or colleagues; inconsistent cover-up stories; or deathbed confessions. And even if they later destroyed all of the lab records, there would likely be paperwork and communications extending far beyond the one site – for materials shipped and received, etc. There would generally be contemporaneous publications or communications with others outside the facility – before those involved would have any reason to dissemble – to disprove their later claims. And subsequent epidemiological or historical research into origins, even if not specifically investigating these claims, would presumably uncover at least some evidentiary threads.

  137. GerrardOfTitanServer says

    But that’s exactly what I’m saying: both of those are essentially unfalsifiable. You can write off everything contradictory to your narrative as “well, they would say that, wouldn’t they”.

    So, you think jury trials are impossible. You also seem to think that eye witness testimony is the most trustworthy kind of evidence. That’s pretty messed up.

    The concept of innocent until proven guilty also applies: if you truly have no independent documentary evidence that can contradict their testimony, you don’t have anything.

    Does this look like a courtroom? No. Courtroom standards don’t apply to my personal opinions about I think happened and their culpability in this matter.

    An assumption that they’re lying isn’t an indictment.

    I’d say it’s more of an informed but tentative conclusion.

    Take this trypsination thing. Right there in front of you, you have the account of experiments by a researcher worker on other stuff, Deinhardt, with no reason to cover up involvement in any horrific infection accident.

    Maybe I read too quickly, but I missed the part where he said that they used trypsin in the Congo. What I just read indicates that they prepared a primitive cell culture in Congo, shipped it overseas, and then applied trypsin.

    There’s plenty of other methodological stuff that’s more or less self-confirming. What about the size of the chimps? It’s stated in there that they were small — almost entirely made up of pre-sexual juveniles, because bigger chimps were too dangerous. That would mean the rate of SIV infection among them would also be quite low, even entirely negligible.

    Is pre-natal infection not a thing in chimps? And again, is there any hard evidence of this, or is this more self-serving personal testimony from those responsible?

    Umm, in the US legal system, the next thing the judge would say, unless a competent prosecutor interjects in here with some kind of case based on concrete facts, would be “good enough. case dismissed.”

    This is not a court of law. There’s also a lot of strong circumstantial evidence that they did it.

    It’s a good deal more than just the core business partners, whoever it is you’re looping into that definition. Table 1 in the Gellin et al paper lists 17 people alone, all testifying to the absence of any use of chimp cultures. Another two are listed in the nearby text. Some of those (Koprowski, Osterreith) are presumably on your list of core conspirators, but some of them are just technicians or grad students, long moved on, who surely would face any personal liability in the matter.

    Anyone who wasn’t in the lab in Congo is likely irrelevant because they would have no knowledge of what actually happened there. Does that list include techs, grad students, and others who were simply in the Wistar institute in Europe? How many worked in the lab in Congo? I’m betting about zero. Those don’t count.

    And that’s just people still alive circa 2001. There were presumably even more potential whistle-blowers in the decades previous. You really do have to be supposing a pretty big conspiracy.

    How so? How many people do you think worked in the Wistar lab in the Congo in Leopoldville? The answer is AFAIK less than 20. Who had access to the inner lab room? Like 2 or 3 or something like that. Who are these whistleblowers that you speak of? Who would they be, and how would they come into possession of critical trade secret information on the creation of the vaccine? That trade secret information would have been kept highly confidential for economic competitive reasons. Their lab notebooks and other recordings were highly secret, just like the other OPV groups at the time. They were in a highly competitive economic race to be the first to create a safer polio vaccine, and the money rewards and fame would have been astronomical. After they discovered their mistakes, they would have even more reason to keep all of that information confidential, and to destroy it – I mean conveniently lose it in a move. “I lost my lab notebooks in a boating accident.”

    You need actual evidence. “They could be lying” is not that.

    According to their own papers and other information, when they gave CHAT OPV in other countries, they amplified it locally. This is circumstantial evidence that they would have done the same thing in Congo. Other OPV vaccine makers of the time also amplified it locally when vaccinating in other countries. We have eye witness testimony of a few African nurses and assistants from the Wistar lab in Congo on video camera claiming that chimp cell cultures were happening. Hooper has other inadvertent and suggestive eye witness testimony that the vaccine was being amplified locally in Congo. We have evidence of hundreds of chimps being sacrificed for as of yet mostly unknown experiments with AFAIK zero published results; the most plausible explanation is that they were used to amplify the vaccine. Hooper has additional evidence that they amplified it locally in Congo. This is pretty strong evidence that they’re lying when they say they didn’t amplify it locally in Congo, and it’s pretty strong evidence that it was amplified locally in chimp cell cultures.

    There is an amazing coincidence in time and place between the first known cases of HIV/AIDS and the CHAT OPV vaccination sites.

    The starburst pattern of the phylogenetic tree is implausible on natural evolution and suggests a something unusual. A real phylogenetic tree looks like this:
    https://cdn.kastatic.org/ka-perseus-images/6a7912e4f113f2e0dde68a8292aa06170e1cff00.png
    It doesn’t have all of its branches coming from the same same point, from a single root. The HIV-1 phylogenetic tree looks rather different. It looks like a tree where all of the branches come from a single root with relatively little branching after the initial “starburst” of branches from that single common root. Multiple crossovers during the CHAT OPV vaccination could explain this pattern. The cut-hunter has great difficulty explaining this pattern. It’s highly implausible that a real phylogenetic tree from typical spread would look like a starburst. For the cut-hunter explanation to explain the starburst, you would need an amazing series of coincidences over the entire spread of HIV-1 in humans between the supposed 1908 or 1920 or whatever crossover point until 1960.

    The geographic dispersion is also a problem. Why did these separate HIV-1 infection lines stay hidden until they all started spreading in Congo in circa 1960? Why didn’t one of the infection lines get to another country and start spreading there instead of Congo?

    The cut-hunter explanation is also not plausible because some of those early cases would have been detected. I believe the testimony of the other doctors above who report that they noticed it early, and that they would have noticed it if it happened earlier, especially with the benefit of hindsight. We have basically zero plausible cases of HIV/AIDS before 1960, and many in the decade after 1960 in Congo. I know, I know, exponential growth, small numbers in the beginning. I’m talking about the supposed middle. Especially in the middle, circa 1950 to 1957, some of these people would have made it to a hospital or a doctor, and their symptoms would have been noticed. Instead, basically no detectable, including post detection, of plausible HIV/AIDS cases in Congo or Africa in general before 1957. I personally believe the testimony of the several doctors that I named above which claim that they would have noticed HIV/AIDS if it existed before 1960, especially from after the fact examination of memories and evidence.

    The idea of non-exponential growth for the first 50 years, as some cut-hunter proponents suggest, in “isolated tribes”, is even more fanciful and ad hoc.

    Much of the lab material including lab notebooks from the CHAT OPV work are claimed to have been lost, IIRC in a move. “I lost my lab notebooks in a boating accident.” More weak circumstantial evidence of wrongdoing. Just like when a cop conveniently forgets to turn on his body camera, these people conveniently lost supposedly exonerating evidence in a move.

    The testimony of the people directly involved in CHAT OPV are inconsistent, evasive, and changing over the years.

  138. GerrardOfTitanServer says

    SC
    That’s exactly the sort of evidence which Edward Hooper has uncovered. His book “The River” has over a hundred pages of references and footnotes. He has tape recording and video recordings of interviews, including nurses and assistants in the lab in Congo who contradict the official story. After just re-reading this followup article, he has found even more such evidence.
    https://web.archive.org/web/20170518092713/http://www.bmartin.cc/dissent/documents/AIDS/Hooper03/Hooper03.pdf
    What you suggest should be found is being found.

  139. GerrardOfTitanServer says

    SC
    See the various conflicting testimony that Hooper has recorded about the presence of chimps, and whether they were sacrificed, and whether serum was made, and whether serum was used to amplify polio vaccine.

    https://web.archive.org/web/20170518092713/http://www.bmartin.cc/dissent/documents/AIDS/Hooper03/Hooper03.pdf

    See also this bit on pages 38 to 39. Basically, according to one paper, the original titre of CHAT pool 10A-11 was 6.7 log doses. According to another paper, the titre of the CHAT pool 10A-11 vaccine used in the Ruzizi trial in Congo was measured at 7.2 log doses. That’s an increase in potency / density. That’s not possible without amplification. However, this small of a difference could fit in the measurement error of the time. However again, one must also include the fact that they had to ship it, which meant an ice box over 3 days. That would mean a substantial drop in titre. This puts the discrepancy well outside the range of measurement error for the time. Smoking gun? No. Another little piece of evidence? Yes.

    Hooper then goes on to cite evidence that basically every other OPV vaccine tester around the world did the same thing – create the initial vaccine in a lab somewhere in the US or Europe, and then ship it frozen or in an ice box to the target third world country for partially-voluntary or involuntary testing. Oral polio vaccine loses potency quite rapidly, even when frozen, and so the several days of air shipping would cause a large in titre, and so they would have to amplify it locally, and they did amplify it locally. Far from an abnormality, this was universally how it was done for oral polio vaccines in the 1950s. CHAT OPV in Congo would be the exception if it was not amplified locally.

    Hooper even has evidence that CHAT OPV was amplified locally when it was used in other foreign countries. According to Koprowski, Congo would be the one exception where it wasn’t amplified locally.

  140. Rob Grigjanis says

    Gerrard: The OPV hypothesis can come crashing down on genetic dating alone. As a non-expert, I’m going with these experts;

    Our results date the origin of the group O radiation to around 1920 (1890-1940), a time frame similar to that estimated for HIV-1 group M. However, group O infections, which remain almost wholly restricted to Cameroon, show a slower rate of exponential growth during the twentieth century, explaining their lower current prevalence. To explore the effect of recombination, the Bayesian framework is extended to incorporate multiple unlinked loci. Although recombination can bias estimates of the time to the most recent common ancestor, this effect does not appear to be important for HIV-1 group O.

  141. says

    According to their own papers and other information, when they gave CHAT OPV in other countries, they amplified it locally. This is circumstantial evidence that they would have done the same thing in Congo.

    From your quotes:

    during this period it was common practice for live polio vaccines to be passaged again in the country which hosted the trials

    …Papers written by Koprowski’s Polish collaborators made no mention of local amplification of the vaccine. However, they revealed that CHAT must have been passaged again in a locally-prepared tissue culture before it was administered.

    I don’t know how to assess his claims about titers, but it’s odd to me that he doesn’t appear to have sought out any more direct evidence to support or refute this conclusion, given how commonplace he’s saying the practice was and the fact that, as he reports, they make no mention of it in their papers. It makes me suspicious of someone’s methods when they form a superficial conclusion they think suits their purpose and then don’t go beyond it. It’s shallow.

    Let’s assume (which we have to do, because he doesn’t take any further steps to present direct evidence of what was done where and how and by whom) that it’s correct that local amplification was common in Europe at the time (I’ll note that he says the first reference he found to local preparation of a Koprowski vaccine was a Yugoslavian article from 1964, “English translation of title and article made by Croatian” [?], which described work from the 1960s). This would have indirect relevance in two senses: first, that if it was the expected practice elsewhere not doing it in Stanleyville would need somewhat more of an explanation (although different practices are often common in one region and not another, and several of the scientists point to the technological and other limitations there) and also because if it was common elsewhere to do it but not to mention it in the literature then it would presumably be easier to hide later in Stanleyville. But again it’s strange to me that, rather than go into a long stretch of fairly speculative hypothesizing about rates of titer loss under varying conditions, he doesn’t look for stronger evidence that this was such a common practice at the time that “It would be odd if Koprowski hadn’t done it” (not that this would prove anything about what he in fact did anyhow). And if it was so common, I have to wonder how was it that he didn’t find articles or communications or guidelines from this period about how best to do it…

    He asks: “So, what of the articles about the vaccinations in the Congo? Do any of them refer to, or hint at, local passage of the virus? They do not.” So he hasn’t definitively shown that “when they gave CHAT OPV in other countries, they amplified it locally” at the time despite not discussing it in their published papers (or personal communications?); there are no contemporaneous references to its having been done in the Congo; the people involved in the Congo say they didn’t do it; and there’s no strong direct evidence that they did do it.

    That’s exactly the sort of evidence which Edward Hooper has uncovered.

    It isn’t.

  142. says

    Still too much nonsense to address it all. Some select responses.

    I asked for a few citations to back claims of the polio vaccine being produced at the Congo lab at the time. I also indicated the conspiracy theory author’s claims weren’t valid citations. Yet that the only ‘source’ I’ve seen Gerrard present on this subject.

    As to recombination nonsense, First I’ll admit the language I used is confusing. Recombinations do result in mutations (and can be considered mutations), but in the context here, recombinations refer to a specific type of recombination event between evolutionary distinct sequences. I’ll rephrase what I wrote before without using the term mutation. ‘Show how using the observed evolution rate (which includes recombination) of HIV-1 is wrong when using its rate in calculations.’

    Gerrard presumable links a few things he thinks he can use to support his case and cherry picks quotes from them.
    @ 3 June 2021 at 7:12 am he links 3 items.
    First is Park, S.Y., Love, T.M.T., Perelson, A.S. et al. Molecular clock of HIV-1 envelope genes under early immune selection. Retrovirology 13, 38 (2016) .
    I’ll quote it myself, the conclusion from the abstract:

    The ability of HIV-1 to escape from immune surveillance in many different directions is the driving force of molecular clock persistence. This finding advances our understanding of the robustness of HIV-1’s molecular clock under immune selection, implying the potential for molecular dating.

    Not in line with what Gerrard would have us believe this paper claims. It’s also looking at intrapatient evolution, not pandemic population evolution.

    Next is Lemey P, Pybus OG, Rambaut A, Drummond AJ, Robertson DL, Roques P, Worobey M, Vandamme AM. The molecular population genetics of HIV-1 group O. Genetics. 2004 Jul;167(3):1059-68. I’ll just quote the abstract:

    HIV-1 group O originated through cross-species transmission of SIV from chimpanzees to humans andhas established a relatively low prevalence in Central Africa. Here, we infer the population genetics and epidemic history of HIV-1 group O from viral gene sequence data and evaluate the effect of variable evolutionary rates and recombination on our estimates. First, model selection tools were used to specify suitable evolutionary and coalescent models for HIV group O. Second, divergence times and populationgenetic parameters were estimated in a Bayesian framework using Markov chain Monte Carlo sampling, under both strict and relaxed molecular clock methods. Our results date the origin of the group O radiation to around 1920 (1890–1940), a time frame similar to that estimated for HIV-1 group M. However, group O infections, which remain almost wholly restricted to Cameroon, show a slower rate of exponentialgrowth during the twentieth century, explaining their lower current prevalence. To explore the effect of recombination, the Bayesian framework is extended to incorporate multiple unlinked loci. Although recombination can bias estimates of the time to the most recent common ancestor, this effect does not appear to be important for HIV-1 group O. In addition, we show that evolutionary rate estimates for different HIV genes accurately reflect differential selective constraints along the HIV genome.

    Bolds mine. Again, not actually something that agrees with Gerrard’s claims.

    And third is Magda Bletsa, Marc A Suchard, Xiang Ji, Sophie Gryseels, Bram Vrancken, Guy Baele, Michael Worobey, Philippe Lemey, Divergence dating using mixed effects clock modelling: An application to HIV-1, Virus Evolution, Volume 5, Issue 2, July 2019. I have no idea why Gerrard even thinks what he quotes supports his position. I’ll quote the abstract again for consistency.

    By analysing a comprehensive HIV-1 group M complete genome data set we confirm considerable rate variation among subtypes that is not adequately modelled by uncorrelated relaxed clock models. The mixed effects clock model can accommodate this rate variation and results in a time to the most recent common ancestor of HIV-1 group M of 1920 (1915–25), which is only slightly earlier than the uncorrelated relaxed clock estimate for the same data set.

    Basically the take home seems to be that science is complicated and scientist know that and account for it. It hardly renders their work faulty as Gerrard would have people believe. This already it too long. If I feel like killing more time on this I’ll write up another post later.

  143. jack lecou says

    Basically the take home seems to be that science is complicated and scientist know that and account for it. It hardly renders their work faulty as Gerrard would have people believe.

    Yeah, I thought I’d written something to this effect, but Gerrard’s word “faulty” is very much not the right characterization. What these calculations are doing is knowingly making some simplifications to make the calculations more tractable. Like ignoring air friction in a ballistics problem. You’ll get a little bit of error, but you know that going in. And it’s an estimate anyway.

    And we can clearly see that the error isn’t that large. All the estimates point back somewhere around 1920. Even if that’s +/-15, it’s more than enough to cause big problems for the OPV theory. (As if it didn’t already have enough. Poor thing.)

  144. GerrardOfTitanServer says

    Rob Grigjanis
    There’s the technical argument which we can skip, but there’s the non-technical argument which is really, really simple. They calculate tMCRA. They assume the MCRA was in a human. Why couldn’t it be in a chimp? Why couldn’t there be multiple crossover events? They’re assuming a single crossover event, which is tantamount to assuming the falsity of CHAT OPV crossover and assuming the truth of the cut-hunter crossover.

    D
    You know I don’t have the kind of evidence that you demand. I have only strong circumstantial evidence which I have already laid out.

    Jack
    It’s not enough to cause problems unless one insists that the the MCRA of each of these strains must be in a human as opposed to in a chimp.

  145. Rob Grigjanis says

    Gerrard @154:

    They assume the MCRA was in a human

    They’re comparing existing gene sequence data. How would any such assumption affect the conclusion? For CoV2019, conspiracy theorists were arguing that it was a manmade modification of RaTG13, which, AFAIK, has only been seen in bat shit. And it was determined that the MRCA for these was about 70 years ago, without any assumptions about where the MRCA was.

  146. GerrardOfTitanServer says

    @Rob
    If one does not assume that the MCRA was in a human, then how is a tMRCA date relevant at all for the debate between cut-hunter vs CHAT OPV as the origin of HIV/AIDS in humans?

  147. GerrardOfTitanServer says

    Rob
    Their argument is: We calculated the tMCRA to be roughly 1908. The MCRA must be in a human (as opposed to a chimp) (equivalently: assume that there was at most one viral crossover from chimp to human.) Therefore, HIV was in humans (1908) before the CHAT OPV Congo trials (1957). Therefore, CHAT OPV Congo trials cannot be the source of HIV/AIDS in humans.

    Without the critical assumption “the MCRA must be in a human”, their conclusion does not follow.

  148. Rob Grigjanis says

    Gerrard @156: If MRCA was 1920, and OPV was late 1950s, how is it not relevant?

    Where is the assumption that MRCA must have been in humans? Seriously, maybe I missed it. Just point it out.

  149. GerrardOfTitanServer says

    Rob

    If MRCA was 1920, and OPV was late 1950s, how is it not relevant?

    I’m sorry. I don’t know how to explain this. One of us is missing something very fundamental. Please explain it like I’m 5. Why should I care if the tMCRA was 1920? Does this disprove CHAT OPV HIV/AIDS hypothesis? How?

    The obvious answer is that if one somehow assumes (or otherwise concludes) that the MCRA was in a human, then one can conclude that HIV was in humans before the CHAT OPV Congo trials, and then one can conclude that the CHAT OPV Congo trials cannot be the origin / cause of HIV/AIDS in humans.

    If you don’t make that critical assumption that the MCRA was in a human, then I don’t see how you can reach that conclusion. The tMCRA date would be simply non-sequitir w.r.t. the CHAT OPV HIV/AIDS origin hypothesis.

  150. says

    There’s the technical argument which we can skip, but there’s the non-technical argument which is really, really simple. They calculate tMCRA. They assume the MCRA was in a human.

    This if false. I asked Gerrard before to show where any of the papers require the assumption of a single crossover to human for the ancestral virus. None provided. Some even have discussions about how it is possible the ancestral virus to pandemic HIV was in chimps and had some expansion and divergence prior to multiple cross over events. That is in fact what the evidence shows for the different HIV-1 groups and HIV-2 (meaning Group M, Group N, Group O and HIV-2 are from different crossovers).

    For the sake of something a little different about HIV origins, I’m going to talk a little about Sauter D, Schindler M, Specht A, Landford WN, Münch J, Kim KA, Votteler J, Schubert U, Bibollet-Ruche F, Keele BF, Takehisa J, Ogando Y, Ochsenbauer C, Kappes JC, Ayouba A, Peeters M, Learn GH, Shaw G, Sharp PM, Bieniasz P, Hahn BH, Hatziioannou T, Kirchhoff F. Tetherin-driven adaptation of Vpu and Nef function and the evolution of pandemic and nonpandemic HIV-1 strains. Cell Host Microbe. 2009 Nov 19;6(5):409-21. doi: 10.1016/j.chom.2009.10.004.
    A short summary of what’s relevant in this paper: Mammals have a cellular protein, referred to as tetherin in this paper, that inhibits enveloped viruses such as HIVs. Pandemic HIV-1 has a protein, Vpu, that counteracts human tetherin very well, and is less effective against chimp tetherin. SIVcpz (thats the SIVs that are in chimps) also has Vpu, but it doesn’t counteract tetherin. Instead, SIVcpz using a different protein, nef, to counter chimp tetherin, but it doesn’t counter human tetherin. HIV-1 nef doesn’t counteract tetherin at all. Pandemic HIV-1s all have the same Vpu motif that allow them to counteract human tetherin, which isn’t present in any known SIVcpz Vpu.
    How’s that relevant to the origin of pandemic HIV? It means that pandemic HIV-1 either originated from an SIVcpz that happen to have this motif (and which there seems to be no selective pressure for in chimps) or quickly acquired after the chimp to human transmission (where there would be very strong selective pressure for this motif). A single low probability cross over event followed by expansion in humans maintaining this Vpu motif is likely because the only barrier is the single cross over. If there were multiple crossovers after expansions in chimps, that would mean either that motif would have been maintained in chimps despite a lack of selection while other non-selected parts of the genome diverged prior to the multiple low probability crossovers or a roughly a dozen low probability cross overs occurred with divergent SIVs that all acquired the exact same motif after the crossover. The single cross over is orders and orders of magnitude more likely the multiple.

  151. jack lecou says

    If you don’t make that critical assumption that the MCRA was in a human, then I don’t see how you can reach that conclusion. The tMCRA date would be simply non-sequitir w.r.t. the CHAT OPV HIV/AIDS origin hypothesis.

    Maybe D can correct me, but I think the main problem is that you’d expect to find a bunch of more closely related chimp SIV variants.

    Your proposal basically implies, I think, that the group M “starburst” happened in chimps, not humans — the vertex of the star is the MCRA, after all. So then in this story, there were a bunch of chimps with some kind of “SIV group M” spinning off multiple “SIV group M” subtypes circa 1920. After spreading for 40 years or so, a bunch of these chimps — with a diversity of “SIV group M” subtypes reflecting the human ones — are collected and taken to Stanleyville to be vaccinated into people. Leading to separate crossovers for each of the corresponding human type M subtypes, circa 1958.

    But if this is so, where are those chimps now? Given how apparently widespread and easily collected these SIV variants were in 1957 or whenever, we would expect to find plenty of them. Some, at least.

    But…Nada.

  152. GerrardOfTitanServer says

    D:
    Finally. Thank you. An argument that I cannot trivially refute. This is now (well) beyond my degree of expertise. Do you have any papers discussing this in the context of CHAT OPV Congo trials and how unlikely CHAT OPV Congo trials could be responsible in light of this new argument – new to me at least? Thanks.

    Jack
    The real argument would be more like this: The dating methods are already pretty hokey, and AFAICT many / most real scientists say that recombination plays havoc with this, and if there was a lot of recombination early on in the starburst pattern, then the dating methods are entirely hopeless. The CHAT OPV hypothesis suggests that there would be a lot of recombination going on while they were amplifying the vaccine locally in chimp culture. There would be ample opportunity from co-caging and from the amplification process itself for lots of SIV from different chimp individuals from different regions in Afirca to all be in the same culture / serum and do lots of recombination.

    So, I’m not suggesting that the starburst pattern is a result of a single origin in chimps which diversified in chimps. That doesn’t explain the starburst pattern. We’re left with the same problem that with natural evolution, starburst patterns like this basically don’t happen. Phylogenetic trees do not look like this. It’s just as unlikely to say it happened in chimps as it happened in humans.

    I am saying for the tMCRA to be relevant, one must assume or otherwise conclude that the MCRA must have existed in a human.

    I’m also saying that the CHAT OPV vaccination process is the moment of the starburst. It’s at this moment where many different SIVs came together with rampant recombination and the resulting soup was given to half a million people. We only need a half dozen or so people to become infected from the vaccination process in order to explain the starburst pattern.

    I haven’t seen a cogent argument against this ever until what D provided in #160 (thanks again). I have no idea how “likely” or “easy” that mutation is. I have no idea how likely it is for SIV to survive in a human body without this mutation (maybe an already weakened immune system?). This is finally something that appears to be a good argument against my position, and I don’t know enough to evaluate it or refute it. At this point, I basically have to stop except for asking for more sources and to do more research myself.

  153. jack lecou says

    hokey..havoc…hopeless.

    You keep saying this stuff, but it’s a transparent misrepresentation. None of that is born out by the literature. It’s fully acknowledged that recombination can throw off the accuracy of the estimates a little, but it’s a known factor and nobody with actual training in the subject seems to think it’s any kind of deal breaker here. A slightly wider +/- doesn’t buy you a plausible tMCRA in 1958.

    And as we saw before, more sophisticated analysis, which brings more sequencing and computation power to bear in order to trace the phylogeny down to individual recombination events…still strikingly agrees with an early tMCRA. Stop. Repeating. These. Claims.

    So, I’m not suggesting that the starburst pattern is a result of a single origin in chimps which diversified in chimps.

    It doesn’t really matter. Either way, the problem is that we should expect to see cousin SIV strains with a tMCRA with group M that’s much closer to 1958. There aren’t any.

    That doesn’t explain the starburst pattern. We’re left with the same problem that with natural evolution, starburst patterns like this basically don’t happen. Phylogenetic trees do not look like this. It’s just as unlikely to say it happened in chimps as it happened in humans.

    This claim was rebutted above. Repeating debunked claims is a hallmark of pseudoscience.

    The ‘starburst’ isn’t some unprecedented mystery requiring an extraordinary explanation. It’s just a mundane multiple founder effect, basically. And the genetic evidence backs that up.

    There would be ample opportunity from co-caging and from the amplification process itself for lots of SIV from different chimp individuals from different regions in Afirca to all be in the same culture / serum and do lots of recombination.

    Which would presumably leave fingerprints, like a bunch of recombinations with tMCRAs ~1960. Not in evidence (on the contrary).

    I’m also pretty sure this just makes the MCRA problem even worse. If SIV strains alpha through gamma (or whatever) all came together in the lab and recombine to make HIV group M babies, then we should expect to find recently diverged (tMCRA=1958) cousins for not just one SIV strain, but a half dozen of them.

    And then:

    Do you have any evidence that particularly large numbers of chimps shared cages? That sexually active chimps were kept in mixed cages?(!) That some or many of them were even old enough to be sexually active? Have you or Hooper figured out how many chimps would need to be there, and caged together, to get the rates of recombination to the necessary levels? (Note that several hundred chimps sounds impressive, but over the course of several years, there wouldn’t have been that many simultaneously on premises at the same time or even had serial contact with each other — camp Lindi reportedly only had facilities for about a dozen. Is a dozen chimps really sufficient for this mass recombination story?) Is there some (any?) evidence that SIV replication or recombination rates go up dramatically with confinement?

    Is there actually any proposed mechanism by which being cultured in kidney cells increases recombination rates? Has Hooper or anyone else tried to test this? Everything we know about those kidney cell cultures says SIV would be lucky to survive in there at all — perhaps just a handful holding out forlornly in a rapidly dwindling reserve of straggler immune cells. It’s hardly an environment for massive replication.

    Nor do I see much opportunity for strains to mix. Maybe I don’t know enough about the process, but I assume each culture is prepared from a single chimp individual – not chimerical. Now if some SIV survives the washing and straining process between amplification steps, I guess it might continue to a new culture (though that assumes cultures from different chimps would have been prepared and be in use simultaneously) and mix with new SIV strains, if any, in that one. But then, that would seem to undermine the latest change in goalposts, which is that the vaccine wasn’t manufactured in Congo, just went through an additional amplification after shipping, prior to safety testing and distribution(*). That’s at least much less, if any, opportunity for strains to mix.

    This whole “lots of recombination happened for some reason” looks like blatant special pleading. Hypothesis doesn’t match the evidence? Propose a whole bunch of new mechanisms no one has ever heard of to patch up the holes.

    I haven’t seen a cogent argument against this ever until what D provided in #160 (thanks again). I have no idea how “likely” or “easy” that mutation is.

    I think this is deeply revealing. That paper is from 2009. If you’re serious about understanding this, maybe you should have found it on your own already, and acquired the expertise to understand it.

    In the meantime, if you don’t deeply understand the issues — as you clearly don’t — maybe you should defer to the actual scientists, who do know about things like how “likely” such a mutation is, or how to interpret tMCRA estimates. Again — not doing so is a hallmark of Dunning-Kruger and pseudoscience crankery.

    Hooper is a journalist, not a scientist. How many actual scientists — people with the expertise to understand and evaluate things like the virus phylogenies — still back Hooper’s hypothesis?

    -——
    (*) I’m just reminded of another question. Why use chimpanzees? I think the explanation Hooper originally gives is that there was at some point a difficulty with obtaining imported monkeys. But that would only ever have applied, if it did, to the Philadelphia or Belgian labs. Now that the accusation has shifted to contamination while manufacturing or amplifying the virus on-site, the question has to be asked again: why chimps? There were reportedly much more plentiful local supplies of baboons and a couple of appropriate monkey species right in Stanleyville, while chimps were comparatively hard to get (they had to be brought in from the other side of the country — and, ahem, not the side closer to the proximal SIV strains, but I digress).

  154. GerrardOfTitanServer says

    D:
    Actually, I have one thing that I remembered. Let me first say that this is pretty speculative.

    HeLa is tenacious, and it has a tendency to infect other cell lines without the practitioners being aware. HeLa contamination was widespread in that era, and I mean truly widespread. What were the numbers again? Maybe half of all mammalian cell lines were actually HeLa at one point in history? It was covered up by the medical establishment for a while, but eventually the truth got out and became widely accepted. (One of the very, very, very rare examples of a seeming wide-ranging conspiracy theory that was actually right. It wasn’t actually a conspiracy theory. Instead, it was just independent but convergent business interests combined with other facets of the medical establishment culture (“face culture”) that refused to see the problem.)
    https://documents.uow.edu.au/~bmartin/dissent/documents/AIDS/Pascal91.html

    We know that they had HeLa lines in the Wistar lab in the Congo.

    What if the vaccine amplification was contaminated with HeLa? HIV can infect and grow in HeLa cells. Vaccine amplification at the time would have been primitive and simple. Likely, they would have taken a seed dose, and amplified it, and taken a new seed dose from the prior amplification and used that new seed for the new amplification. They were constantly adding new chimp cells possibly infected with HIV, and HeLa contaminates everything around it all on its own even when good care is taken to prevent it. That could explain how SIV became adapted to human cells. The amplification plus vaccination process I describe here could explain the starburst pattern that we observe, and this other aspect could solve the problem of how so many different SIV lines became adapted to humans, aka became HIV – recombination. It would take just one success to infect a HeLa cell, and recombination would handle the rest.

    I believe that it’s public uncontested knowledge that the Staneyville lab in Congo had HeLa lines. There also appears to be other weak evidence of CHAT OPV being passaged through HeLa strains.
    https://documents.uow.edu.au/~bmartin/dissent/documents/AIDS/Hooper03/Hooper03a.pdf

    Again, even now I’m sounding like a crackpot to myself, and I recognize this, but I still find the overall CHAT OPV hypothesis fascinating and compelling in spite of your good argument against it. I don’t think your evidence is fatal, and I don’t know if this HeLa diversion actually helps my case, but it might. Take this as you will.

  155. GerrardOfTitanServer says

    D:

    I think this is deeply revealing. That paper is from 2009. If you’re serious about understanding this, maybe you should have found it on your own already, and acquired the expertise to understand it.

    It’s a side hobby that I haven’t looked at it over 10 years in any serious detail. Sue me.

    None of that is born out by the literature.

    I thought I supplied papers above which say that much of the earlier dating papers didn’t even consider recombination, which means it applies to these earlier papers – papers which were wrongly used as disproof of CHAT OPV HIV/AIDS. For these later papers that I’ve just become acquainted with thanks to you (thanks again), I don’t know. I haven’t had time to review them. I’m not an expert in the exact area, but being something of an information specialist and computer science specialist, I’m suspicious of the claims that large amounts of recombination early on in the history could be properly detected and accounted for.

    It doesn’t really matter. Either way, the problem is that we should expect to see cousin SIV strains with a tMCRA with group M that’s much closer to 1958. There aren’t any.

    Now you’re just speaking bullshit. We have done nowhere near enough testing of native chimp populations to make that sort of proclamation. Stop speaking obvious nonsense.

    Further, we wouldn’t need such a thing if the CHAT OPV scenario is true because the large amount of recombination in the amplification process would likely greatly obscure any connection from HIV-1 to any SIV.

    The ‘starburst’ isn’t some unprecedented mystery requiring an extraordinary explanation. It’s just a mundane multiple founder effect, basically. And the genetic evidence backs that up.

    So, 6+ founders. Of a novel RNA retrovirus. With basically zero evidence of the mere prior existence of any of the 6 founder strains in humans. That all appeared in exactly the same time and place (concerning HIV-1) and didn’t appear anywhere else. This is far from mundane. How many other multiple founder examples do we have of 6+ founders? How many of those involve cases where we cannot find any evidence of the existence of any of the 6 founders prior to the multiple founding event? How many other multiple founder example do you have where ancestor populations of the founders didn’t previously branch out somewhere else?

    Which would presumably leave fingerprints, like a bunch of recombinations with tMCRAs ~1960. Not in evidence (on the contrary).

    I’m sorry. Where in the papers did they make any such claim?

    Everything we know about those kidney cell cultures says SIV would be lucky to survive in there at all perhaps just a handful holding out forlornly in a rapidly dwindling reserve of straggler immune cells. It’s hardly an environment for massive replication.

    If you say so. I’m unconcinved. I am unaware of any testing. It would be really useful if anyone did such experiments.

    Nor do I see much opportunity for strains to mix. Maybe I don’t know enough about the process, but I assume each culture is prepared from a single chimp individual – not chimerical.

    You’re making a lot of assumptions about the process based on modern safety standards which I sincerely doubt were practiced back then.

    But then, that would seem to undermine the latest change in goalposts, which is that the vaccine wasn’t manufactured in Congo, just went through an additional amplification after shipping, prior to safety testing and distribution(*). That’s at least much less, if any, opportunity for strains to mix.

    Get a grip. This is like the only major change to the hypothesis, and the hypothesis was changed like 30 years ago. This is what good science does. It adapts to new evidence.

    This whole “lots of recombination happened for some reason” looks like blatant special pleading. Hypothesis doesn’t match the evidence? Propose a whole bunch of new mechanisms no one has ever heard of to patch up the holes.

    That’s what HIV does. It does a lot of recombination. This isn’t special pleading. This is just facts.

    Hooper is a journalist, not a scientist. How many actual scientists — people with the expertise to understand and evaluate things like the virus phylogenies — still back Hooper’s hypothesis?

    No idea.

    why chimps? There were reportedly much more plentiful local supplies of baboons and a couple of appropriate monkey species right in Stanleyville, while chimps were comparatively hard to get (they had to be brought in from the other side of the country — and, ahem, not the side closer to the proximal SIV strains, but I digress).

    Chimps were still dirt cheap. Why chimps and not other species? Dunno. I could look over Hooper’s collected evidence, but it doesn’t seem to be important to know why the decision was made. 400 chimps were purchased, used, and killed for something.

    Hooper is a journalist, not a scientist.

    Just adding the label “scientist” to someone does not automatically make them trustworthy. The onus is on all of us to evaluate our experts to see if they are trustworthy. Given the unethical behavior that I have seen from the few scientists who are most active against the CHAT OPV theory, I simply don’t trust them. The earlier dating papers were obviously nonsense, and yet they attempted to use them as a disproof of CHAT OPV. That’s basically dishonest. They also tested a sample of vaccine from Europe which had never been in Congo, and they tried to use that as a disproof of CHAT OPV, and they still do, in spite of the many, many years after the one change in the hypothesis, and this behavior is also dishonest. I’m not accusing you of dishonesty, but some of these publishing scientists really ought to have done better, and these specific scientists no longer get automatic trust from me like most publishing scientists do.

  156. GerrardOfTitanServer says

    D:
    I mean, we could also play the game of cite-a-paper.
    http://www.aidsorigins.com/wp-content/uploads/rs_burr.pdf

    The subtypes of human immunodeciency virus type 1 (HIV-1) group M exhibit a remarkable similarity in their between-subtype distances, which we refer to as high synchrony. The shape of the phylogenetic tree of these subtypes is referred to as a sunburst to distinguish it from a simple star phylogeny. Neither a sunburst pattern nor a comparable degree of symmetry is seen in a natural process such as in feline immunodeciency virus evolution. We therefore have undertaken forward-process simulation studies employing coalescent theory to investigate whether such highly synchronized subtypes could be readily produced by natural Darwinian evolution. The forward model includes both classical (macro) and molecular (micro) epidemiological components. HIV-1 group M subtype synchrony is quantified using the standard deviation of the between-subtype distances and the average of the within-subtype distances. Highly synchronized subtypes and a sunburst phylogeny are not observed in our simulated data, leading to the conclusion that aquasi-Lamarckian, punctuated event occurred. The natural transfer theory for the origin of human acquired immune deficiency syndrome (AIDS) cannot easily be reconciled with these findings and it is as if a recent non-Darwinian process took p lace coincident with the rise of AIDS in Africa

    So, “tag, you’re it”, in this game of cite-a-paper. I’m curious if you can find something to the contrary, or if the authors of my source are – unknowingly to me – cranks. I’m not an academic, and I don’t know how to (quickly) verify the credentials of a publishing scientist.

    I’ll also try to look for papers that contradict this.

    PS: Hah. The paper cites “The River” by Hooper as for certain kinds of background evidence. Say what you will about Hooper, but his ability to do certain kinds of historical research seems to be unparalleled.

  157. GerrardOfTitanServer says

    PPS:
    I didn’t properly say the real complaint. The real problem is not the starburst pattern. Multiple founders could plausibly explain that. The real problem is that all 8~ strains at the end of the starburst are equidistant. I don’t think multiple founders can explain that. The paper goes into this in more detail better than I ever could.

  158. says

    @ Jack
    4 June 2021 at 10:56 am

    You are essentially correct. If the polio vaccine did cause the human introduction of Group M HIV-1 by recombination of SIVs to create the various subgroups, then those parental SIV would have had to existed extensively. While we have found SIVcpz that is closely related to Group M, they aren’t closer to some subtypes than others, as would be expected from the vaccine transmission proposal. You are also correct that such a transmission event would leave genetic evidence that doesn’t seem to exist, but we can always offer proponents of the conspiracy theory to provide it. If one believed that pandemic HIV-1 was the result of vaccine transmitted chimeras and had a passable understanding of phylogeny and recombination (as Gerrard claims to have), they could analyze the same sequences used by others to determine the MRCA and show extant subtypes are chimeric and determine the parental sequences, which should be matchable to at least some different SIV sequences. I’ll not be holding my breath for that.

    @ 4 June 2021 at 6:22 pm Gerrard

    What if the vaccine amplification was contaminated with HeLa? HIV can infect and grow in HeLa cells

    HIV-1 can’t infect HeLa cells unless they’ve been modified to express CD4.

    Again there’s just too much wrong with Gerrard’s comments, much of which has already been shown to be wrong (repeatedly), but which he isn’t willing to understand.

    I’ll also point out that I am not Jack. and vis versa.

  159. GerrardOfTitanServer says

    Again there’s just too much wrong with Gerrard’s comments, much of which has already been shown to be wrong (repeatedly), but which he isn’t willing to understand.

    What makes you think that? I’m trying to be open-minded. I’ve admitted when you raised an argument which is a good argument which I have no obvious firm counter to.

    Also, what’s wrong with the paper that I cited? There are a few scientists on the side that it’s at least plausible. What are these experts getting wrong in their modeling?

  160. GerrardOfTitanServer says

    D:
    And you’re still wrong about the state of knowledge of SIV. The number of SIV samples that we have are staggeringly small. Making any broad claim like (paraphrase) “we’ve found the ancestor” or “we won’t find another SIV that has these other properties” is grossly premature.

  161. GerrardOfTitanServer says

    D:
    So, are you relying on Korber? I have another paper here that suggests that Korber spectacularly failed in their paper when they tried to find and remove all recombinants. This new paper also echoes what I’ve been hearing from other places – that no, it’s not easy to tell if a data set had lots of recombination early on. Rather the opposite – it’s difficult or impossible to tell.

    What makes you think you could have scientists look at a data set and be able to determine that lots of recombination happened early in the history before the MCRA, and be able to determine the time to MCRA? This seems to contradict everything that I can find. There was one paper above which I think suggested otherwise. Which paper was that again? I want to try to read it again.

    https://www.bmartin.cc/dissent/documents/AIDS/Schierup03.pdf

    Previous phylogenetic studies have tried to circumvent effects of recombination by filtering out detectable recombinant sequences, but it is unclear to what extent this approach alleviates the problem, since recombination within subtypes and recombination events happening early in the evolution are very difficult, if not impossible, to detect, while they may still have important consequences for phylogenetic analysis (Wiuf et al. 2001).

    […] the second data set we have analyzed has been actively “cleaned” for signs of recombination (Korber et al. 2000). Table 2 shows that this data set still appear to show signs of recombination both within and between subtypes. Recombination within subtypes is not surprising since the method used to remove recombinants only works for between-subtype recombinants, but the magnitude of the estimated recombination rate is surprising. A greater surprise is the evidence of recombination (apparently at a very high rate) between subtypes. This is important, because it indicates that recombination may have been prevalent also before the diversification into subtypes, i.e. early on in the evolution of the present diversity. Note that none of the R2 tests for this data set are significant. This may reflect that the cleaning-for-recombinants process has detected sequences, which are compatible with different trees in different regions (and thus contribute most to the correlation detected by R2). It may also reflect that recombination is so prevalent that the R2 test loses power when applied to the longer sequences of the Korber set.

  162. GerrardOfTitanServer says

    Let me go back into so-called crazy-town. I repeat that this is wild speculation. I wish I had some non-biased experts to talk to, and I wish someone would do this experiment.

    https://www.bmartin.cc/dissent/documents/AIDS/Hooper03/Hooper03.pdf

    l) The potential significance of HeLa contamination.

    The fact that chimpanzee cells (which may well have been SIV-contaminated) appearto have been used to make human vaccine in Stanleyville in the period up to April1958 is, in itself, alarming. But if such vaccines, in turn, were subsequentlycontaminated with, or passaged in, or diluted by, HeLa cells, then this couldpotentially have been far more serious in terms of the impact on human health.

    Although much work has been done on the natural history of HIV in the human body(and of SIV in the bodies of primates), many details, such as the precise mode of viralentry, remain uncertain. What is clear, however, is that both lymphocytes andmacrophages are prime target cells for HIV and SIV. However, there is a difference,for SIV-infected lymphocytes have one furious burst of virus production in vitro, andthen die off. By contrast, SIV-infected macrophages continue throughout the life of aculture to spew SIV out into the supernatant.202 Macrophages do not die off and, asRobin Weiss has observed, they make up approximately 1% of all epithelial cellcultures.203 They are sometimes referred to as cellular vaccum cleaners.

    So let us imagine a chimp cell culture of which one part in a hundred is made up ofSIV-contaminated macrophages, which is then combined with cells that are describedas KB, or FL, or ERK-1, but which are in fact HeLa. Is it conceivable that SIVcpzcould grow in HeLa? When I first asked this question of microbiologists andvirologists back in the late nineties, most of them said that this could only happen in agenetically engineered cell line, such as HeLaT4+, which was not created until the1980s. But is that really the only way?

    What follows in the next two paragraphs is sheer speculation, for I can find nothing inthe literature about whether or not SIVcpz will grow in a HeLa culture – or, indeed,about what impact HeLa might have on the chimp virus, if it did support its growth.

    Some microbiologists I have spoken with believe that because macrophages arefusogenic, the act of transferring chimp cells containing macrophages into HeLa, thatmost turbocharged of tissue cultures, could in itself generate a hybrid cell line whichwould combine chimp CD4 cells with the immortality of HeLa. They say that such ahybrid cell line would, from that point on, represent an excellent substrate for growingSIVcpz (for instance if SIVcpz-contaminated tissue culture was introduced into theHeLa/chimp hybrid). Furthermore, they say, the necessary process might be evensimpler, and require just a single step – that of putting primate cells which containedalready SIV-infected macrophages into HeLa. However, in this instance the outcomeis less readily forecastable, in that the hybrid cells might spew out SIV, or might bekilled off by the SIV.

    If such a hybrid HeLa/chimp cell line was accidentally created in the course of theCHAT vaccine research that was taking place in the Congo during the fifties, then thepotential implications could have been “a recipe for disaster”, in the words of onerespected microbiologist. Such a cell line could introduce a crucial amplification stepto the basic OPV theory, by allowing the mooted chimp SIV contamination of CHATto become human-adapted. Furthermore, if two or more SIVs were present in aHeLa/chimp hybrid culture, they would be likely to recombine even more rapidly thanin a chimp cell substrate. [For the potential implications of such recombinations, see“Dating the epidemic”, below.]

    I must repeat that such analysis clearly remains in the realm of the hypothetical – atleast until such time as someone stages an appropriate in vitro experiment.

    The basic OPV theory, involving a contaminated chimpanzee tissue culture used tomake the polio vaccines fed in the Congo, stands up on its own. However, if HeLacontamination of those cultures also occurred, this just might represent the “extra ingredient”, the amplification step, that could help to explain why this particularzoonotic transfer was some orders of magnitude more serious, in terms of humandisease, than those other SIV transfers which resulted in the human outbreaks of HIV-2, and HIV-1 Groups O and N. These latter three outbreaks may have resulted fromcontact with bushmeat, or from iatrogenic (possibly polio vaccine-related) episodes[see below] in west Africa and west central Africa, but they have probably resulted infewer that 20,000 fatalities in total.204 By comparison, by 2002 the Group M-relatedAIDS pandemic seems to be some three orders of magnitude greater, having causedan estimated 20 million deaths.

  163. GerrardOfTitanServer says

    Peer reviewed paper from 2012.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258043/

    Moreover, given our inability to account for the discrepancies between the subtype tMRCAs and the combined HIV-1 M analysis, we feel less confident in the inferred tMRCA of HIV-1 M. And based on our simulations, one might expect the true tMRCA of HIV-1 M to be younger than previously inferred.

    One other comment I want to make. OPV may be responsible only for HIV-1M, aka the vast majority of infections. Other strands, such as group O, may be from cut-hunter, or other polio vaccines, or some other source. I think the calculated times to MCRA are much closer to 1960 when considering only group M and not all HIV strains. CHAT OPV hypothesis seeks primarily to explain only the HIV major group strains, and not all strains. Ex:

    https://www.nature.com/articles/35400

    Our results, the rate of HIV-1 evolution (around 0.005–0.01 nucleotide changes per site per year17) and previously described methods of estimation of evolutionary rates24 indicate that the major-group viruses that dominate the global AIDS pandemic at present shared a common ancestor in the 1940s or the early 1950s. Given their ‘starburst’ phylogeny, HIV-1 was probably introduced into humans shortly before that time frame, about a decade or two earlier than previously estimated17,25. Thus, given the large genetic distance between HIV-1 and HIV-2, the divergence of these viruses could not have occurred in the late 1940s (ref. 25); that branching point must have been considerably earlier17,26,27,28.

  164. GerrardOfTitanServer says

    D:
    Also, regarding this paper posted above by D. Bolding added by me.
    Faria NR, Rambaut A, Suchard MA, Baele G, Bedford T, Ward MJ, Tatem AJ, Sousa JD, Arinaminpathy N, Pépin J, Posada D, Peeters M, Pybus OG, Lemey P. HIV epidemiology. The early spread and epidemic ignition of HIV-1 in human populations. Science. 2014 Oct 3;346(6205):56-61
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254776/

    Our analyses robustly place the spatial origin of the HIV-1 group M pandemic in Kinshasa [posterior probability (PP) = 0.99] (Figs. 1 and ​and2).2).

    Explanations (ii) and (iii) are compatible with an early establishment of group M in high-risk groups of small size—for example, commercial sex workers with higher rates of partner exchange and/or exposure to contaminated injections—before later spreading to the larger, general DRC population from the 1950s onward. Specifically, the transition to faster exponential growth (Fig. 4) agrees with available public health data (34) and the hypothesis that transmission rates of group M increased as a result of the administration of unsterilized injections at sexually transmitted disease clinics in the 1950s and/or subsequent changes in the nature of commercial sex work in Kinshasa from the early 1960s, which led to increased client numbers (34). The idea that early HIV spread included an iatrogenic component is supported by data from other blood-borne viruses.

    So, in order to fit the data, the virus spread rate tripled circa 1960. Further, these authors say that it probably included an iatrogenic cause aka caused by physicians and medical practice. They suggest increased use of unsterilized needles. CHAT OPV proponents suggest it was another iatrogenic cause: using chimp organs to amplify an oral polio vaccine. How funny that these authors are baby steps away.

    Even under the unsubstantiated assumption that the spread rate was 3 times less before circa 1960, that still means thousands of cases in Leopoldville / Kinshasa before 1960. There were good doctors there who would have noticed this, but they didn’t. Absence of evidence is not evidence of absence, but absence of expected evidence is evidence of absence. You can’t have good doctors somehow miss thousands of cases in a city and the neighboring areas. No such cases exist in the medical records nor the doctor’s memories.

    This paper is shooting themselves in the foot. If you look between the lines, you see the contortions that the anti-OPV scientists have to go through.

    See Hooper’s response.
    http://www.aidsorigins.com/more-supportive-of-opv-aids-than-of-the-bushmeat-hypothesis-a-revised-response-to-the-recent-faria-paper-in-science/

  165. jack lecou says

    I thought I supplied papers above which say that much of the earlier dating papers didn’t even consider recombination, which means it applies to these earlier papers – papers which were wrongly used as disproof of CHAT OPV HIV/AIDS.

    “Didn’t even consider” is your pejorative gloss, but what does it mean? There’s “fail to consider” — like they don’t even know about recombination. And then there’s “decide not to consider”. Only the former would be a fatal flaw, and all of the papers I’ve seen are the latter — they are deliberately choosing to do a simpler calculation, and are upfront about their assumptions and the possible loss of precision. Like ignoring air resistance in a ballistics problem.

    The early ones may not have been the strongest disproof for that reason, but the genetic evidence has only continued to pile up. At this point it is very powerful evidence against the OPV hypothesis, and you need to reckon with that.

    Now you’re just speaking bullshit. We have done nowhere near enough testing of native chimp populations to make that sort of proclamation. Stop speaking obvious nonsense.

    I only said it hasn’t been found. And it hasn’t. I don’t know what the actual odds are that it wouldn’t have been encountered are yet, if it exists, but chimp SIV has been surveyed quite extensively — sequences are collected from the wild via fecal samples. Hundreds of SIV variants have been catalogued. We even have multiple SIV strains closely related to group M. But all with common ancestors prior to 1920. Why nothing after that?

    Under the OPV hypothesis, the lab’s sources apparently had no trouble obtaining dozens if not hundreds of such samples (literally every infected chimp purportedly used). Where are they now?

    Further, we wouldn’t need such a thing if the CHAT OPV scenario is true because the large amount of recombination in the amplification process would likely greatly obscure any connection from HIV-1 to any SIV.

    I’ll need a lot more than just your assertion on that. It doesn’t obscure the family relation between type M and the supposedly less related SIV ancestor variants we know about. Why should it obscure even more closely related ones? That’s just grasping at straws.

    So, 6+ founders. Of a novel RNA retrovirus. With basically zero evidence of the mere prior existence of any of the 6 founder strains in humans. That all appeared in exactly the same time and place (concerning HIV-1) and didn’t appear anywhere else. This is far from mundane. How many other multiple founder examples do we have of 6+ founders? How many of those involve cases where we cannot find any evidence of the existence of any of the 6 founders prior to the multiple founding event? How many other multiple founder example do you have where ancestor populations of the founders didn’t previously branch out somewhere else?

    You need to read that paper. I literally don’t know what you’re talking about with “cannot find evidence for the existence”. All the strains are still in and around Congo. The diversity is higher there, and the pattern of variation matches normal evolution there – the so-called “subtypes” more or less blur together, in fact. It’s the variants that traveled outside Congo that exhibit sharper differentiation. Founder effect. This is all in the paper. And I’m not sure why you think there’s a limit on the number of founders. I’m sure a lot more than 6 people took trains out of Kinshasha in the ’30s or whenever, though maybe only around that many with HIV did.

    And while we’re here:

    I mean, we could also play the game of cite-a-paper.

    Literally taken straight from your ‘counter’ paper:

    Another possible synchronizing event could be a local outbreak in one African region that later spread distinct, but still closely related, variants of the virus to other parts of Africa and finally to the rest of the world. These distinct variants could then act as seeds (founders) for what later became classified as the different subtypes. The recent discovery of previously uncharacterized M group sequences in Central Africa lends considerable support to the natural origin hypothesis (Vidal et al. 2000) with a synchronizing local outbreak.

    IOW, the very possibility the other paper investigated more deeply and found to be well supported.

    Both of these papers are from way back ~2001, I think, so I’d be happy to see some followups with more sequences and a deeper analysis, but unless something extraordinary came up, I think the matter can be considered closed.

    I’m sorry. Where in the papers did they make any such claim?

    The one that has a bunch of recombinant tMCRAs in the 20s, 30s, and 40s, but no error bars that even span 1960.

    If you say so. I’m unconvinced. I am unaware of any testing. It would be really useful if anyone did such experiments.

    One might even say absolutely necessary to support Hooper’s hypothesis…

    You’re making a lot of assumptions about the process based on modern safety standards which I sincerely doubt were practiced back then.

    Not modern safety standards. Just economy. One kidney will make a lot of cultures — and you get two kidneys from each chimp. Why would you be using dozens of different chimp cultures together at the same time? Two maybe, as you get near the end of one batch and start the next.

    Get a grip. This is like the only major change to the hypothesis, and the hypothesis was changed like 30 years ago. This is what good science does. It adapts to new evidence.

    Well, that and this new HeLa hypothesis. And who knows what else.

    What good science does when a hypothesis fails is to go back to the drawing board and check every assumption carefully. What Hooper does when a hypothesis fails is continue to assume his original suspicions were correct in the general, if not the specific, then dig ever more desperately for some other way they might possibly, maybe still be true.

    But he’s never actually had the slightest iota of hard evidence that chimp cultures were used in the first place. Only suspicions based on a splashy, headline grabbing accusation, and leaps of fancy based on nothing more than conspiratorial readings of any remotely ambiguous note or statement. What Hooper does is not science.

    That’s what HIV does. It does a lot of recombination. This isn’t special pleading. This is just facts.

    It doesn’t just suddenly do a lot more recombination than usual, in the obscure circumstances that are conveniently necessary to satisfy Hooper’s suspicions.

    Certainly not to anyone else’s knowledge anyway. If he wants to actually provide the evidence for this process of accelerated recombination…

    Chimps were still dirt cheap. Why chimps and not other species? Dunno. I could look over Hooper’s collected evidence, but it doesn’t seem to be important to know why the decision was made. 400 chimps were purchased, used, and killed for something.

    Sure. In the OPV context, many were regularly killed in the course of testing neurovirulence (a use for which they do actually make more sense then cheaper primates).

    That lab also did a lot of work on a ton of stuff other than OPV, too though, remember. Malaria, yellow fever, bacterial diseases. Deinhardt was using chimps quite intensively in hepatitis research, apparently, in addition to his infamous six airmailed kidneys. I don’t know the entire list of things chimps might have been useful for back then, but it all seems perfectly well accounted for so far as records or recollections can be expected to that far back. The use of a bunch of chimps in support of this kind of lab at that time and place seems to me the very opposite of suspicious.

    So why does Hooper insist on finding it so?

    Hooper’s conspiratorial thinking and desperate grasping at straws really poisons everything, you know. He seizes on things like access to the chimp site being somewhat restricted (for safety and hygiene purposes – a perfectly cromulent thing) or Osterrieth working alone in his lab (there’s certainly an element of racism to his exclusion of his assistants, if I’m reading the subtext, but he would also have a perfectly cromulent impulse to keep delicate work safe) as evidence for some kind of secret plot.

    But what secret? If the OPV hypothesis is true, they didn’t know to cover it up at the time!

    And if they did know that using chimp cultures was wrong, why not just use even cheaper baboons and monkeys. Hooper’s suspicions are literally circular.

    You can’t just brush the ‘why’ question under the rug. Chimps were more difficult to obtain. Chimps were in fact already known to be a higher risk for human pathogens. Monkeys were being used in the US and Belgian labs. Even assuming on-site amplification (unproven) it makes absolutely no sense for them to have used chimps when baboons and monkeys were, if anything, even more available.

    Just adding the label “scientist” to someone does not automatically make them trustworthy. The onus is on all of us to evaluate our experts to see if they are trustworthy.

    You’re missing the point. I’m not saying all scientists are automatically trustworthy. I’m saying Hooper lacks the training to evaluate the science. And he lacks the temperament to investigate his claims thoroughly or objectively.

    I’ve been reading some of Hooper’s own words, and it’s really terrible.

    One of the primary triggers for his investigation was apparently some shoddy correlations he ran between towns where early infections can be traced, and towns where OPV was administered:

    Through 1981, there are 70 instances of African Group M infection that can be linked to a city, town or village, of which 30% come from Kinshasa. However, there is a far stronger correlation, for 76% of these infected sera were obtained from places where CHAT vaccine was fed in the late fifties.

    Nowhere do I see any evidence that he’s subjected this — then or since — to any actual statistical tests. What are the chances that 70 cases could have this distribution by chance? Hooper doesn’t know. Or care. And has he considered any alternative hypotheses? For just one example, which occurred to me within about half a second of reading that, what if these towns are more likely to both receive vaccine and uncover cases (or have taken sera samples that could be later tested) because of some quirk in health care infrastructure that they share? You guessed it, Hooper didn’t check. It’s not clear he’s ever even thought about that.

    And he’s relentlessly manipulative:

    Koprowski – in collaboration with researchers from the Belgian Congo – had just opened a huge chimpanzee research station (Mission Courtois Koprowski: Centre d’Experimentation) at a place called Lindi

    “Huge chimpanzee research station”? Please. Lindi was, by all accounts, a couple of shacks with wooden cages for about a dozen chimps (separate cages, by the way – bad news for all that recombination).

    But it’s a “huge research station” for Hooper because he needs it to be big and sinister in the next paragraphs, where he’s grasping for some way to answer the question I ask above: why they would have used chimps for vaccine amplification, despite every reason not to. Hooper’s best guess? Because they’ve got all these chimps they don’t know what to do with and need to justify their “huge chimpanzee research station”.

    That’s actually — no kidding — one of the things that he says made him suspicious in the first place. He never stopped and re-evaluated after finding out the “huge chimpanzee research station” maybe wasn’t quite so grand.

    And what was the other thing? That’s even more amazing:

    The first reason was that a short while before he developed CHAT, Hilary Koprowski had inaccurately reported the substrate in which he had prepared his previous Type 1 polio vaccine, SM N-90. In three articles published in 1956 and 1957, Koprowski reported that he had been using a tissue culture of chick embryo, when in fact he had been using one of monkey kidney. The reason for this misrepresentation is still not clear.

    Yikes. I’m really not sure what’s supposed to be suspicious about this, even in Hooper’s suspicious mind. A mistake was made, obviously. Some notes were mistranscribed. A persistent brain worm was exorcised. Something. It happens.

    But to Hooper it’s definitely already a “misrepresentation”. What is Hooper’s suspicion? The best I can infer is that I guess he thinks Koprowski was already secretly using chimp kidney (for reasons left entirely unexplained) and wants to hide it (for reasons left entirely unexplained) but is too dumb to just write “monkey kidney” in his lab notes (for reasons left entirely unexplained).

    This is some fake moon landing level conspiracy garbage.

    There is a lot more where that came from. I literally can’t open a single page where Hooper isn’t transparently heaping significance on something like one tiny word — or even the lack of a word — and leaping from there to unsubstantiated suspicion and thence to new heights of unsubstantiated suspicion. At one point (I can’t remember if it was in this volume, or some other one I was looking at) he even has the gall to complain about how his interview subjects appear to clam up on subsequent sessions. He seems unaware that others might be able sense what an obvious hatchet job he’s trying to work on their words.

    If you’re truly interested in this “hobby” as you call it, I would encourage you to re-read Hooper’s own words, with a larger helping of critical salt than perhaps you used the first time, and see what you truly make of them.

    Given the unethical behavior that I have seen from the few scientists who are most active against the CHAT OPV theory, I simply don’t trust them. The earlier dating papers were obviously nonsense, and yet they attempted to use them as a disproof of CHAT OPV. That’s basically dishonest.

    You’re just swallowing Hooper’s spin on it. But those earlier dating papers weren’t nonsense in the slightest. If not quite disproof, and that’s arguable, they were certainly very strong evidence against Hooper’s hypothesis, which, along with all the other revelations and retreats, was eminently dismiss-able by that point. I don’t blame anyone on the other side of his…journalism…for wanting to close the case as firmly as possible.

    They also tested a sample of vaccine from Europe which had never been in Congo, and they tried to use that as a disproof of CHAT OPV, and they still do, in spite of the many, many years after the one change in the hypothesis, and this behavior is also dishonest.

    His original accusations certainly included European and American vaccines. There’s still no actual evidence any vaccine was made in the Congo, so I’m not sure how they were supposed to have tested samples of that. This is basically a “when did you stop beating your wife” objection from Hooper.

    I’m not accusing you of dishonesty, but some of these publishing scientists really ought to have done better, and these specific scientists no longer get automatic trust from me like most publishing scientists do.

    I did not and do not say you need to trust these specific scientists. What you need to do is trust other scientists, at least provisionally. When a paper comes out that says something like “HIV crossed over in 1920” or “HIV’s starburst phylogeny can be explained by founder effects” you should probably provisionally accept that they — and the reviewers of the paper — are learned people who have already implicitly considered and rejected a hundred more highly technical angles of potential objection than you even know might exist. You should at the very least not just immediately run it through the “but Edward Hooper says…” filter and assume that it’s flawed work.

    That doesn’t mean you need to accept their word forever, of course. It’s fine and good to go read up very thoroughly, and perhaps come back with a solid reason to object to their conclusions. But you really need to be sure you know at least as much as they do first. Dunning-Kruger is a tricky mistress.

  166. jack lecou says

    So, in order to fit the data, the virus spread rate tripled circa 1960.

    There’s a lot of research on this. The cultural and colonial factors and changes that patterned HIV’s spread, from 1920 onward. It’s extremely interesting stuff if you’re not just mining it for quotes to (badly) make a pro-OPV argument.

    <

    blockquote>Further, these authors say that it probably included an iatrogenic cause aka caused by physicians and medical practice. They suggest increased use of unsterilized needles. CHAT OPV proponents suggest it was another iatrogenic cause: using chimp organs to amplify an oral polio vaccine. How funny that these authors are baby steps away.

    If you think those things are at all similar looking — “baby steps away”? I can’t even.

  167. says

    I see Gerrard is still dishonestly quote mining papers that counter his claims to spin them as supporting them.

    I’m not going to repeat refutations of the conspiracy theory that have already been ignored, misapprehended or misrepresented by Gerrard.

    I will again restate that the conspiracy theory has no positive evidence for it. It has wild conjecture based on supposed correlations, fantastical speculations and outright falsehoods. Beyond a few scientists taking it seriously prior to the early-mid 2000s (not entirely unreasonable at the time), the conspiracy theory has since been considered soundly rebuked by the field.

  168. GerrardOfTitanServer says

    D:

    I will again restate that the conspiracy theory has no positive evidence for it.

    Correlation in time and space between vaccination sites and first known HIV samples and AIDS cases. Motive and opportunity. Having hundreds of chimps killed on site (lots of evidence for this). Need to amplify vaccine on site (lots of evidence for this). A complete lack of HIV samples and AIDS cases before 1968 in Congo in spite of thousands of cases supposed to exist before 1957. That is all evidence. Saying it has no evidence is just silly. It shows your extreme bias in the matter. You don’t need to make such a strong claim to dismiss it, but you go above and beyond. You’re not being objective or reasonable. That taints everything that you say. I don’t consider anything you say to be reliable.

    Jack:
    I don’t see the genetic evidence as strong evidence against. I still have yet to see any proper argument that multiple crossovers could not explain the genetic evidence (but I have seen the argument that multiple crossovers are less likely). I have seen sources saying that recombination very early on in the diversification of HIV would be practically undetectable, and mere assertions by D to the contrary.

    You say that we have hundreds of SIV samples from the wild? Do you mean hudnreds of distinct SIV strains from like 8 individual chimps? Or from hundreds of individual chimps? As best as I can tell with an insufficient amount of searching, there are only 8 wild chimps who have been sampled as positive for SIV. So, I have no idea what you’re talking about. 8 individuals from all of Africa is a woefully small number – insufficient to make any such pronouncements AFAIK.

    You’d only need a couple of SIV infected individual chimps in the OPV CHAT hypothesis plus recombination to explain the present diversity of the M group.

    Why use multiple chimp kidneys? Because they likely seeded the next batch/pool from the previous batch/pool.

    He has no evidence of chimps being used? He has hard evidence of 400~ chimps being there, and killed, and eye witness testimony that their organs were harvested. Is this hard evidence? Why do I need to fulfill whatever arbitrary criteria that you’ve set up? I only need to show 1- it’s plausible, and it is, and 2- it’s more plausible than the ridiculous cut-hunter hypothesis.

    You say that they were doing a lot more research at the Stanleyville camp. AFIAK, this is based almost entirely on the testimony of the individual scientists who I already claim are lying. There was little to no significant amount of research results from any of the supposed research.

    Chimps were in fact already known to be a higher risk for human pathogens.

    Absolute nonsense. You have no idea what you’re talking about. SV-40 came as a huge shock to everyone.

    The earlier dating papers – when used as a disproof of OPV – were absolute nonsense because they didn’t evne mention the possibility of multiple crossover events and explicitly stated that they were going to ignore the effects of recombination, some with token effort to remove recombinant strains but later papers showing that they did a very bad job doing so.

    There’s plenty of evidence that they amplified vaccine in Congo because that’s what Koprowski et al did when it was administrated in every other country, and because that’s what all of the other OPV groups were doing at the time. They had to. Even on ice, the vaccine lost titre very quickly, in a matter of days.

    I should trust these other scientists, but what about the other other scientists that I cited which said the opposite? It’s now just a game of “cite a paper”. How does one “win?”. I don’t have the necessary knowledge to critique the fine details, but I can tell that there are lot of shenanigans going on from one side but not the other.

    If you think those things are at all similar looking — “baby steps away”? I can’t even.

    I don’t get it. What’s your point? Both hypotheses were accidental medical interventions. The best dating methods from the cut-hunter side apparently rely on the entirely proven assumption of a massive iatrogenic event which drastically changed the reproduction rate of HIV in humans. If they get to pull unsubstantiated guesswork out of their ass, why are you complaining when the CHAT OPV side purportedly does? Some of the pro cut hunter people admitted that their dating techniques don’t produce sensible results unless they assume a massive human intervention circa 1960. If that’s not even a little suspicious, then I don’t know what to say to you.

    http://www.aidsorigins.com/more-supportive-of-opv-aids-than-of-the-bushmeat-hypothesis-a-revised-response-to-the-recent-faria-paper-in-science/
    Fractally wrong.

    Well. I don’t see anything obviously wrong from another skim. I’d like to know what you think is so obviously wrong, but barring that, I guess you should write me off as too thick headed and too full of myself to listen. You’re not going to get anywhere by saying “I or someone else know better than you” especially when it doesn’t involve highly technical matters, but I’m willing to listen to real arguments.

    PS:

    Dunning-Kruger is a tricky mistress.

    Didn’t it come out recently that the original Dunning-Kruger paper was severely flawed?

  169. GerrardOfTitanServer says

    Typo:

    The best dating methods from the cut-hunter side apparently rely on the entirely unproven assumption of a massive iatrogenic event which drastically changed the reproduction rate of HIV in humans.

  170. says

    GerrardOfTitanServer @ 6 June 2021 at 7:54 pm

    Correlation in time and space between vaccination sites and first known HIV samples and AIDS cases.

    Correlation does not demonstrate causation. That tenet of logic is so basic I have to wonder at anyone willing offering up such a statement. Even taken as circumstantial, how strong is it? I’ve not seen any real attempt to make more than a very vague hand waving correlation, not even basic epidemiological linking.

    Motive and opportunity.

    Being vary charitable that this is a claim about simply producing OPV at the Congo labs and not introducing SIV into humans, this is speculation. Motive for wanting to have the capacity to make OPV on site is somewhat reasonable to assume. Opportunity is speculation contrary to statements of the researchers. One would need some good evidence to show the Congo labs actually had the facilities to manufacture OPV at the time for this not to be wild speculation. And even if by chance such evidence was provided, motive and opportunity to produce OPV would still be circumstantial.

    Having hundreds of chimps killed on site (lots of evidence for this).

    No one is disputing the Congo labs had chimps. Again this is circumstantial and very week. Having/killing chimps is neither necessary nor sufficient for making OPV. There is no corroborated evidence they were used for OPV manufacture and evidence against such. Wild conjecture.

    Need to amplify vaccine on site (lots of evidence for this).

    False.

    A complete lack of HIV samples and AIDS cases before 1968 in Congo in spite of thousands of cases supposed to exist before 1957.

    Also false, which anyone with even a passing knowledge and understanding of the field would know. Even if true, it would again just be circumstantial.

    So again. No. Positive. Evidence.

    And speaking of things one with just a passing knowledge and understanding of the field would know or be able to quickly find out, from Sharp PM, Hahn BH. Origins of HIV and the AIDS pandemic. Cold Spring Harb Perspect Med. 2011;1(1):a006841. doi:10.1101/cshperspect.a006841:

    Collective analyses of nearly 2,000 wild-caught or captive-born apes identified fewer than a dozen SIVcpz positive individuals (Sharp et al. 2005)

    and

    At select field sites, mitochondrial and microsatellite analyses of host DNA were also used to confirm sample integrity and to determine the number of tested individuals. Figure 3A summarizes current molecular epidemiological data derived from the analysis of over 7,000 chimpanzee fecal samples collected at nearly 90 field sites (Santiago et al. 2002, 2003; Worobey et al. 2004; Keele et al. 2006; Van Heuverswyn et al. 2007; Li et al. 2010; Rudicell et al. 2010). These studies have identified common chimpanzees as a natural SIVcpz reservoir, but also revealed important differences between the epidemiology of SIVcpz and that of other primate lentiviruses.

    I’ll forgo again refuting the other repeated falsehoods that have already been shown to be wrong.

  171. GerrardOfTitanServer says

    Another typo.

    A complete lack of HIV samples and AIDS cases before <b1957 in Congo in spite of thousands of cases supposed to exist before 1957.

    Sorry for the typo. After the fix, this is true. No confirmed cases of HIV by blood test before 1957. Practically zero cases of AIDS strongly indicated by symptoms before 1957. This is the simple truth.

    The further truth is that if the outbreak was centered in Leopoldville / Kinshasa circa 1960 as indicated by the latest cut hunter peer reviewed papers, and if there were a thousand HIV positive human individuals prior to 1960 as indicated by the same papers, then one can conclude that they must be wrong. That number of infected persons would definitely been noticed by the western doctors working there circa 1950 and onwards. What we do have are: No blood samples. No doctor notes or reports. No doctor recollections. And positive doctors recollections that there were no such patients.

    I did say approx 8 wild chimp individuals have directly tested positive for SIV which is supported by what you just cited. I didn’t mention the feces testing in part because the feces samples all come a similarly small number of sites, and thus also indicating a very small number of tested individual wild chimps. You have given nothing to contradict this. You’ve just given evidence to support what I said. Why do you think what I said on this issue is wrong?

  172. jack lecou says

    You say that we have hundreds of SIV samples from the wild? Do you mean hudnreds of distinct SIV strains from like 8 individual chimps? Or from hundreds of individual chimps? As best as I can tell with an insufficient amount of searching, there are only 8 wild chimps who have been sampled as positive for SIV. So, I have no idea what you’re talking about. 8 individuals from all of Africa is a woefully small number – insufficient to make any such pronouncements AFAIK.

    Demonstrating once again, a deep ignorance and incuriosity.

    Here’s just one single paper finding 76 SIV positive individuals in a set of over 2,500 samples. Just the first paper at the top of a simple google search. There are many others.

    Like I said, I have no idea what the actual odds are that any candidates for the missing SIV lineages haven’t been found. There may be big swathes of habitat with poor survey coverage still (inaccessible due to wars or other reasons, perhaps). It is also possible the chimps in question have simply died out.

    But it certainly does seem improbable to me. Again, these lost strains were apparently much less hidden as recently as the late 50s — all of the multiple purported OPV sources would have had to have come from these now vanished viral lineages. And on the other hand, we’ve already found at least two or three SIV strains that are strikingly consistent with a crossover in the early part of the century (superficially, they’re only something like 80% homologous, but IIRC, that’s very close to what you’d expect after so many decades of divergent evolution — the tMCRA with HIV is sometime in the late 1800s, with error bars that actually overlap with many of the estimates for the HIV-1 M tMCRA – they’re potentially the closest living relatives we’d expect to find). Either those were just super lucky, or it is really pretty weird that we haven’t found anything consistent with a purported event almost 60 years closer in time to us.

    Also as D said, if there’s actually some mathematically alternative phylogenetic interpretation, put it in a paper. If Hooper had a leg to stand on, collaborating on some actual peer reviewed research would be far more fruitful and convincing than a thousand additional speculations about the sinister hidden meaning in a misplaced word by an 80 year old interview subject or whatever.

    Instead, he’s out there ignorantly casting FUD on the entire field of viral phylogenetic dating. To a laughable degree — somewhere in one of the recent links he’s scoffing at “relaxed” clock models because I guess he thinks “relaxed” is a synonym for sloppy — he obviously doesn’t have the faintest clue. And it’s no wonder the editors at Nature and Science don’t take his calls anymore. None of this is how scientists, even serious amateurs, work. It’s exactly how creationists and other pseudo-scientists work though…

    Why use multiple chimp kidneys? Because they likely seeded the next batch/pool from the previous batch/pool.

    You don’t keep the kidney cells — or any other cells (like, say lymphocytes) — after making a passage, just the filtered virus.

    In any case, the total number of kidneys required for all of the virus administered in Congo is on the order of 12, even if they did that all at once (rather than over the course of months or years), that’s only about 6 chimps potentially being cross-contaminated for this magical hyper-recombination scenario. (And what fraction of them would even have been SIV-positive?)

    He has no evidence of chimps being used? He has hard evidence of 400~ chimps being there, and killed, and eye witness testimony that their organs were harvested. Is this hard evidence? Why do I need to fulfill whatever arbitrary criteria that you’ve set up? I only need to show 1- it’s plausible, and it is, and 2- it’s more plausible than the ridiculous cut-hunter hypothesis.

    I despair. What I said very clearly is that he has absolutely no evidence of chimp cultures being used [for OPV amplification]. Obviously there were chimps there — everyone agrees there were chimps there. I mentioned in that very post that there were chimps there. They needed them for, among miscellaneous other things, research on whether the OPV’s neurovirulence had been sufficiently attenuated.

    You and Hooper do indeed need to prove that they weren’t put to the dozen other uses, most of which were documented at the time. Otherwise,
    claiming that the mere presence of chimps — and extraction of their organs for various examinations — is somehow suspicious in and of itself is ludicrous. It’s an insult to intelligence. (And yet these flimsy leaps of suspicion are the links Hooper’s entire chain is pieced together from. Tug on it and it doesn’t fail in one place, but almost every place.)

    You say that they were doing a lot more research at the Stanleyville camp. AFIAK, this is based almost entirely on the testimony of the individual scientists who I already claim are lying. There was little to no significant amount of research results from any of the supposed research.

    If you’re getting that from Hooper, he’s straight up lying, and not very intelligently.

    Neither the lab nor the chimp facility were private Wistar operations, you know. Courtois worked for the Belgian colonial public health authority, and all the facilities were theirs. The Belgian authority even paid for a major upgrade and expansion ca. 1958 or so. As a government facility, and presumably one of very few in the region, it would have been responsible for carrying out research in support of all kinds of public health work in the colony. The documentation is in any number of old requests and activity reports, in addition to plain common sense.

    Absolute nonsense. You have no idea what you’re talking about. SV-40 came as a huge shock to everyone.

    I’m sure it was upsetting, but it was hardly surprising. This conference paper, from at least a year prior to the SV40 discovery, mentions that explicit testing for possible simian viruses in vaccine production was standard practice by that time. It also raises concerns that the testing methods then available might not be sufficient (which, alas, was soon proven to be the case).

    I don’t have any solid citation that chimpanzees were considered extra suspicious, but the mid-50s wasn’t the stone age, and I’m assuming it was well recognized that chimps were one of the more — if not most — closely related primates to humans, and that this also might make them more likely to share certain diseases than more distantly related ones. It’s not rocket science. The close homology of chimps was presumably one of the main reasons they had become (to the poor chimps’ misfortune) a preferred lab model for research into neurology, into human diseases like hepatitis — or OPV neurovirulence for that matter — etc. If that’s not the case, I think you can go ahead and show me something.

    There’s also the perennial dilemma here: Hooper, time and time again, relies on purported hints of a contemporaneous conspiracy to fuel his suspicions. Sinister mislabeled lab notes, secret nocturnal lab work, off limits chimp cages, etc. etc. But there was nothing secret about using monkeys and other primates in poliovirus cultures at the time, however regrettable in retrospect. What else would they have had to hide, if not chimps specifically? (And if there’s a reason to hide them, why use chimps when other primates were at least as easy to work with, and were certainly used for production and development elsewhere…around and around we go.)

    The earlier dating papers – when used as a disproof of OPV – were absolute nonsense because they didn’t evne mention the possibility of multiple crossover events and explicitly stated that they were going to ignore the effects of recombination, some with token effort to remove recombinant strains but later papers showing that they did a very bad job doing so.

    Mentioning a weird multiple crossover hypothesis isn’t those papers’ job. It doesn’t affect the math either way. They did explicitly (thank you) neglect recombination, or take only simple efforts to account for it. They more or less had to, at the time, as genetic sequencing was still in early days and additional techniques — and the computational power to perform them — weren’t available yet. AFAICT, despite later papers showing the full importance of recombination had perhaps been less well understood than initially thought, the actual numeric range of the estimates in this case has held up very well. This is all just the way science works. There is literally nothing to fault them for.

    Of course, Hooper doesn’t care. He needs to attack the field with pseudoscientific vehemence. Not because the science is bad. But because, as with the creationists, the science is his enemy.

    There’s plenty of evidence that they amplified vaccine in Congo because that’s what Koprowski et al did when it was administrated in every other country, and because that’s what all of the other OPV groups were doing at the time. They had to. Even on ice, the vaccine lost titre very quickly, in a matter of days.

    Maybe. It would have been packed in dry ice, and Osterrieth says the trip, with a stop in Belgium, took a maximum of 48 hours, which is eminently plausible. Air travel was a thing in the 1950s, you know. Evidence of local amplification from other countries is circumstantial at best — it might have depended on the quality of the facilities that were available, for example, which were probably much better in Poland than Congo.

    And then, that’s still just amplification. And you actually need to show two parts simultaneously, amplification [in Congo], and amplification in chimp tissue. Even if there was local amplification, why not in monkey cultures? Why would they have risked changing procedures from what was tried and true in the states?

    I should trust these other scientists, but what about the other other scientists that I cited which said the opposite? It’s now just a game of “cite a paper”. How does one “win?”. I don’t have the necessary knowledge to critique the fine details, but I can tell that there are lot of shenanigans going on from one side but not the other.

    It’s not a game of ‘cite a paper’ if you actually read the papers, and try to understand their contents rather than just quotemining them. AFAICT, I’ve more than adequately rebutted every one of your ‘citations’ — often with elucidation drawn from elsewhere in the very same papers.

    The only shenanigans you’ve demonstrated so far is your own willingness to dive into this debate without sufficient mastery of the science.

    I don’t get it. What’s your point? Both hypotheses were accidental medical interventions. The best dating methods from the cut-hunter side apparently rely on the entirely [un]proven assumption of a massive iatrogenic event which drastically changed the reproduction rate of HIV in humans.

    Again you haven’t read the paper. I guess that’s my job now?

    It’s the difference between an aggravating factor and an instigating factor. There’s no “massive iatrogenic event” being hypothesized, or in evidence.

    However, there are demonstrably a multitude of well known aggravating factors in HIV transmission, of which needle hygiene is only one. Another is sexual behavior. So we might expect a difference in transmission rate between relatively monogamous contexts, and places like colonial boom towns full of workers and prostitutes. Congo and the neighboring areas is anything but static during the time period in question, so the prevalence and importance of all these factors vary as the virus spreads to different places and as the cultural, technological, political and economic situation changes.

    In short, these hypotheses you think are ‘steps away’ are not remotely related, nor do they look the same in the record.

    (Also, what’s “unproven” about needle sharing — or, say, blood transfusion — as a vector for HIV transmission? I’m pretty sure that there are multiple documented instances of both. Rather unlike a certain hypothetical instance of cross-species transfer of SIV in an oral polio vaccine.)

    Well. I don’t see anything obviously wrong from another skim. I’d like to know what you think is so obviously wrong, but barring that, I guess you should write me off as too thick headed and too full of myself to listen.

    Well, let’s see:
    – He starts with a few paragraphs of well poisoning. Scientists are on their back feet trying to salvage a failed theory, and/or out to get him. It’s a conspiracy, and journals refuse to publish his own shoddy, rehashed theory. Yada, yada. Typical pseudoscience crank-y kind of complaints. (I’d point out that some of the scientists involved with this paper probably haven’t even heard of him, nevermind being out to get him. but I don’t want to hurt his feelings.)

    Asserts that the crossover event is an “unjustified assumption” rather than the only thing so far consistent with the (phylogenetic) evidence. I really don’t think it’s the job of every single paper to explicitly point out how the evidence doesn’t support his personally preferred discredited alternative. (He’d probably complain if they did, in fact.)
    Complains churlishly about the author’s use of contemporary place names [emblematic of his failure to even try to understand the paper — but we’ll get to that later]
    Spends a couple of paragraphs putting an outsized significance on precise years given, as if these are exact dates. To him, the fact that the paper refers to “1920” as a date for the viruses introduction to Kinshasa represents “a tectonic shift” from other sources giving 1908 as the date of the crossover event in Cameroon. 12 years and 500-odd miles apart. Somehow this is a conflict, because, I guess, he thinks that what everyone thought before that was that HIV spread to all the big cities in SE Cameroon first [hint: there are none], rather than go straight downriver into the Congo, where the strongest evidence for the earliest outbreaks has always been. [I got dumber just reading those paragraphs. ‘Tectonic’ my left hoof.]
    more complaints about molecular clocks — again, essentially attempting to discredit a whole field of science (this isn’t just used in HIV research, you know). And it’s effectively just math — this is qualitatively no different from someone who complains that people keep publishing papers where 2+2=4, and he really, really, wants 2+2 to be 5. They haven’t considered the possibility, you see.

    Anyway, he starts by complaining that phylogenetics assumes HIV mutates at a constant rate — although then in the very next paragraph he also complains about relaxed molecular clocks. Hilarious. It’s more like that. There’s no technical criticism here. Just, apparently, that the problem with relaxed molecular clocks is that they don’t give results he likes [“by providing results to underpin their assertions, behaves as they want it to behave”. Maybe it’s just that their assertions actually match the evidence, Ed. It does tend to make the science easier.] He quite plainly has failed to read the paper, or certainly understand it. He talks about their justification of their molecular clock models as being comparable to “giving Ghengis Khan a couple paragraphs to explain himself”. Well, unlike him, I clicked through to the supplementary material, so let’s check it out:

    All five data sets (fig. S1, table S1) were analyzed using a general time-reversible (GTR) nucleotide substitution model (71) specifying a gamma distribution as a prior on each relative substitution rate, with a shape parameter = 0.05 and a scale parameter = 0.10 for all rates except for rAG, for which a scale parameter of 0.20 was specified. We used a discrete gamma distribution to model among-site rate heterogeneity (72) with an exponential prior (mean = 0.5) on the shape parameter. We used a relaxed uncorrelated lognormal (UCLN) molecular clock model in order to infer the timescale of HIV evolution while accommodating among-lineage rate variation (73), with a gamma distribution prior on the mean clock rate (shape = 0.001, scale = 1000) and an exponential prior (mean = 1/3) on the standard deviation.

    To confirm that our results are robust to the choice of the molecular clock model, we estimated the time of the most recent common ancestor (TMRCA) for data set C using (i) the UCLN model (73), (ii) the strict molecular clock, which assumes no among-lineage variation, (iii) the uncorrelated exponential relaxed clock (UCED) (73), and (iv) the random local clock (RLC) model (74), which allows a small number of discrete rate changes and hence permits different regions of the tree to evolve under different evolutionary rates. Crucially, all give highly consistent estimates (fig. S8a) demonstrating that the estimated epidemic timescale is robust to the molecular clock prior model chosen. No support was found for phylogenetically- correlated rate changes under the RLC (95% CIs of the estimated number of discrete rates = 0-4). The coefficient of variation of the UCLN, a measure of among-lineage rate variation, was estimated at 0.229 (95% CI: 0.198-0.259). We also tested whether estimates of the TMRCA, and of the age of the ZR59 strain used for statistical validation, were congruent across the data sets analysed. Estimates of these dates were highly consistent across data sets A, B, C and D (fig. S9).

    To reconstruct the spatial dynamics of HIV-1 group M, we employed a Bayesian discrete phylogeographic approach (75, 76) using Markov chain Monte Carlo (MCMC) sampling, as implemented in the BEAST v1.8.0 software package (77). We also used the BEAGLE parallel computation library (78, 79) to enhance the speed of the likelihood calculations. For each data set, at least 3 MCMC chains of 250 million steps were computed. Parameters and trees were sampled every 50,000th step. Samples were combined with LogCombiner (77) and between 10 to 30% of each MCMC chain was discarded as burn-in. MCMC mixing was diagnosed using visual trace inspection and calculation of effective sample sizes in Tracer (77). We report the posterior mean and 95% Bayesian credible intervals for evolutionary parameters. Using LogCombiner, we subsampled the posterior distribution of phylogenetic trees to generate an empirical distribution of 2,000 trees that is representative of the posterior sample. These were used for the phylogeographic analysis reported in Tables S2-S5. Sequence alignments, accession numbers, BEAST XML input files, and subsampled tree files are available in the DRYAD Repository (http://dx.doi.org/10.5061/dryad.nn952).

    Sure sounds like something Ghengis Khan would write to me!

    The next thing, and frankly the first thing so far that might even sound convincing at first glance, is an attempted gotcha about travel and city sizes. But this only further demonstrates that he hasn’t read or understood the paper in the slightest.

    His objection is that the paper lists Brazzville, Lubumbashi and Mbuji-Mayi as the top three population centers with the greatest early spread from the epicenter in Kinshasa. But, “a ha!”, he says, Mbuji-Mayi was Bakwanga back in the day, and Bakwanga was less populous than Kinsangani, which didn’t make their list (it was — it was the fourth biggest destination — but Hooper doesn’t bothers to mention that little detail). Further, he says, based on his trusty 1956 travel guidebook, travel was easier to Kinsangani. He seems to think this is grounds for dismissing the whole thing — partly because it seems like he genuinely believes it’s just “cut-hunter” hacks making up some imaginary markings on a map, and he thinks he’s caught them in a major flub.

    But this actually takes us back to those contemporary city names he was complaining about earlier. Do you know why they use those names instead of old colonial equivalents? It’s a clue. It’s because that’s where the modern sample data came from. If I understand it right, I believe the gist of what the paper is doing is taking a bunch of cases, like, say, one from the area of modern Mbuji-Mayi, and phylogenetically tracing their relationships to all the other samples in other places. Those relationships let you infer a temporospatial probability distribution about the most likely locations and times where they their ancestors were in the same place. They found, among other things (and I’d encourage you to read the whole thing, including the supplement, it’s very impressive stuff, — certainly orders of magnitude more convincing than Hooper’s innumerate eyeballing of AIDS cases and vaccine sites), that the areas represented by the three modern cities named before were major early destinations for virus traveling from Kinshasa, with Kinsangani in 4th.

    In other words (and frankly this should have been obvious to him), it’s not about technicalities like people’s official street addresses. It’s about the general population center for that area. Back in the colonial era, Mbuji-Mayi was called Bakwanga, and Bakwanga certainly was relatively small. But there were other places nearby. Like Lusambo, perhaps, which is a relative backwater now, but right on the river, and a provincial capital and important military post back in the day. It has equal pride of place on old maps with Kinsagani. (I don’t have population numbers from the ’20s or ’30s, but eyeing the street grids in the older parts of towns, it looks like it could have been around the same kind of size.) There are also several other towns in the area which may have been more important back in the day, but are now subsumed in the “Mbuji-Mayi” sample, maybe literally, as the city grew in importance and gobbled up nearby populations.

    As to travel, well, I don’t think Hooper’s 1956 ferry schedules are particularly relevant. The critical times for early geographic leaps appear to be more in 20s and 30s, maybe 40s. Things like ferry schedules would have been changing quite a bit between 1920 and 1956. It seems like the fact that Lusambo was right on a navigable river all along may be an important fact. And the authors’ source for confirming transport links is an old book, in French, on colonial transportation infrastructure, with data on changes through the entire relevant era (notably, it’s not “internet searches” as Hooper snidely suggests, having apparently not done the slightest due diligence). I’m going to assume they at least halfway know what they’re talking about and not waste any more time.

    I’m also going to stop there and not go through the rest of the whole thing, because it’s equally terrible, and this really isn’t my job. You need to develop some critical reading skills of your own.

    Didn’t it come out recently that the original Dunning-Kruger paper was severely flawed?

    By whatever name, I think we have plenty of field trials — many on this very blog — that demonstrate some such phenomenon exists.

  173. jack lecou says

    Even on ice, the vaccine lost titre very quickly, in a matter of days.

    I covered it already, but want to reiterate that this one, like so many others, is very much [citation needed]. Modern polio vaccines are stable for weeks at even a couple of degrees above freezing. IIRC, they keep quite a while at, say, -20C. I recognize that they aren’t the same, but even so, dry ice is -78C. Are we really supposed to believe it couldn’t keep for two days?

  174. jack lecou says

    Here’s a contemporary paper on the actual vaccination program, with relevance to both the supposed amplification hypothesis and the rate of loss of titre:

    The vaccine arrived in LUopoldville in the frozen state with a concentration of 107.5 TCD50 of virus per ml. In Leopoldville the vaccine stock was divided into small vials, each containing 1 ml, which were kept in a freezer at – 20°C. On the day of vaccination the contents of a 1-ml vial were diluted in 300 ml of neutral saline solution. The final concentration of the vaccine was therefore 105-0 TCD5o per ml. For infants less than 30 days old 1 ml of concentrated vaccine was diluted to 20 ml in a medicine dropper bottle, giving a final concentration of 106.2 TCD50 per ml.
    The 300-ml bottles and the medicine dropper bottles of diluted vaccine were both kept on ice at 0°C throughout their subsequent use for vaccination. Any vaccine remaining in the large bottles was discarded at the end of the day, whereas the contents of the small bottles for infant use were used for two days. The titre of the vaccine after a day’s use was checked periodically by sending frozen aliquots to the Wistar Institute, Philadelphia, Pa., USA. Titration of these samples showed good maintenance of virus titre.

    A rather detailed description of the entire supply chain and procedure, yet curiously no mention of any amplification, in chimpanzees or otherwise. And apparently not only did the vaccine titre hold up well enough for travel to Congo, the way they kept track of the titre of doses used in the field was to freeze samples and send them back all the way back to Philadelphia.

    But I guess obviously they’re just lying. In 1959. For some reason. Maybe Doctor Who went back in time to warn them to get a coverup ready?

    No. This isn’t a hypothesis that is merely pining for the fjords. It is no more. It has ceased to be. It is bereft of life. It rests in peace. It is an ex-hypothesis.

  175. says

    Just quickly while I have another moment to kill.
    @ 7 June 2021 at 2:48 am
    Gerrard again demonstrates his deficiencies in reading comprehension and/or honesty.
    From what I quoted @ 6 June 2021 at 11:30 pm from Sharp PM, Hahn BH. Origins of HIV and the AIDS pandemic. Cold Spring Harb Perspect Med. 2011;1(1):a006841.

    Figure 3A summarizes current molecular epidemiological data derived from the analysis of over 7,000 chimpanzee fecal samples collected at nearly 90 field sites

    Bold mine.
    Gerrard’s response:

    I didn’t mention the feces testing in part because the feces samples all come a similarly small number of sites, and thus also indicating a very small number of tested individual wild chimps.

    I won’t bother with the continued wild conjecture presented as if it is evidence.

  176. GerrardOfTitanServer says

    Jack
    Re fecal samples. Thanks for preemptively correcting yourself. It’s not direct samples thousands of individual chimps. It was thousands of fecal samples from a relatively small number of sites. Only a small number tested positive. Since you’ve read the paper, is that consistent with the idea that all of the positive samples came from a small subset of the tested sites? If so, that’s entirely consistent with a very small number of tested individual wild chimp individuals.

    And again, if you want peer reviewed papers, I don’t think I’ve seen you reply to this:
    http://www.aidsorigins.com/wp-content/uploads/rs_burr.pdf
    Again, multiple-founders cannot explain the HIV tree. Multiple-founders cannot explain 8~ branches that are all equidistant from each other. They ran simulations and could not produce a tree quite like the HIV tree.

    Again, to be clear, you accept that the cut hunters are proposing a massive iatrogenic “aggravating” event circa 1960, right? You’re just mad that I didn’t make enough verbal distinction between originating event and aggravating event, right? Ok. Whatever. Also, again, the source where the cut hunter proponents make the claim:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254776/

    Back to you:

    I really don’t think it’s the job of every single paper to explicitly point out how the evidence doesn’t support his personally preferred discredited alternative. (He’d probably complain if they did, in fact.)

    Again, it is their job when many of those papers are explicitly claiming this as disproof of OPV, and it’s explicitly the job of the scientists outside of the paper to consider this possibility when citing these papers as disproof of OPV. What you’re saying here is nonsense. These scientists were behaving grossly incompetently or dishonestly when they were using the earlier dating papers as disproof of OPV.

    PS:
    I still completely unsatisfied by the dismissal of my argument that someone would have noticed the thousand HIV infected individuals before 1960. It’s suggested by the latest cut hunter papers that most of these infected people were in Congo, and if so, at least some of them would have been detected by the (western) doctors that were there before 1960. However, there were no such detected cases. Saying “oh it would just present as normal pneumonia or TB” shows great ignorance of how HIV/AIDS actually presents. Saying “but there weren’t enough good doctors and hospitals” also shows ignorance of the state of affairs in Congo circa 1950.

  177. jack lecou says

    Re fecal samples. Thanks for preemptively correcting yourself. It’s not direct samples thousands of individual chimps. It was thousands of fecal samples from a relatively small number of sites. Only a small number tested positive. Since you’ve read the paper, is that consistent with the idea that all of the positive samples came from a small subset of the tested sites? If so, that’s entirely consistent with a very small number of tested individual wild chimp individuals.

    For pity’s sake. Go read back. I specified fecal samples in the post that kicked off this whole SIV samples discussion.

    There’s nothing special about a direct sample, except being stressful for the chimp. You can obtain perfectly good viral RNA sequences from the poo. You can also sequence the chimp DNA to figure out how many distinct chimps you sampled. There’s obviously some overlapping, but 7000 samples still represents an awful lot of sampled chimps. Read the papers yourself for a change.

    And again, if you want peer reviewed papers, I don’t think I’ve seen you reply to this:
    http://www.aidsorigins.com/wp-content/uploads/rs_burr.pdf
    Again, multiple-founders cannot explain the HIV tree. Multiple-founders cannot explain 8~ branches that are all equidistant from each other. They ran simulations and could not produce a tree quite like the HIV tree.

    I will quote my earlier reply, verbatim:

    Literally taken straight from your ‘counter’ paper:

    Another possible synchronizing event could be a local outbreak in one African region that later spread distinct, but still closely related, variants of the virus to other parts of Africa and finally to the rest of the world. These distinct variants could then act as seeds (founders) for what later became classified as the different subtypes. The recent discovery of previously uncharacterized M group sequences in Central Africa lends considerable support to the natural origin hypothesis (Vidal et al. 2000) with a synchronizing local outbreak.

    IOW, the very possibility the other paper [the one this paper of yours was supposed to counter] investigated more deeply and found to be well supported.

    Satisfied?

    Again, to be clear, you accept that the cut hunters are proposing a massive iatrogenic “aggravating” event circa 1960, right?

    No.
    Scientists who study the issue have been looking into the ways known social factors that influence HIV propogation waxed and waned throughout the whole period. The needle re-use is pretty horrific, but it’s only one of many factors, and nothing started suddenly in 1960 or anything. It was a continuous process.

    Again, it is their job when many of those papers are explicitly claiming this as disproof of OPV, and it’s explicitly the job of the scientists outside of the paper to consider this possibility when citing these papers as disproof of OPV. What you’re saying here is nonsense. These scientists were behaving grossly incompetently or dishonestly when they were using the earlier dating papers as disproof of OPV.

    No, they were right.

    Hooper doesn’t like it, but that doesn’t make 2+2=5.

    I still completely unsatisfied by the dismissal of my argument that someone would have noticed the thousand HIV infected individuals before 1960.

    Tough.

    I’m not satisfied with the way Hooper is starting to preemptively poison the well about potential future retrospective cases early than 1957 by dropping hints that “conspirators” might fake the provenance of specimens. This is positively Trumpian. (What conspirators, even? The supposed conspiracy was 80 years ago, and pretty much everyone is dead at this point.)

  178. jack lecou says

    Re fecal samples. Thanks for preemptively correcting yourself. It’s not direct samples thousands of individual chimps. It was thousands of fecal samples from a relatively small number of sites. Only a small number tested positive. Since you’ve read the paper, is that consistent with the idea that all of the positive samples came from a small subset of the tested sites? If so, that’s entirely consistent with a very small number of tested individual wild chimp individuals.

    For pity’s sake. Go read back. I specified fecal samples in the post that kicked off this whole SIV samples discussion.

    There’s nothing special about a direct sample, except being stressful for the chimp. You can obtain perfectly good viral RNA sequences from the poo. You can also sequence the chimp DNA to figure out how many distinct chimps you sampled. There’s obviously some overlapping, but 7000 samples still represents an awful lot of sampled chimps. Read the papers yourself for a change.

    And again, if you want peer reviewed papers, I don’t think I’ve seen you reply to this:
    http://www.aidsorigins.com/wp-content/uploads/rs_burr.pdf
    Again, multiple-founders cannot explain the HIV tree. Multiple-founders cannot explain 8~ branches that are all equidistant from each other. They ran simulations and could not produce a tree quite like the HIV tree.

    I will quote my earlier reply, verbatim:

    Literally taken straight from your ‘counter’ paper:

    Another possible synchronizing event could be a local outbreak in one African region that later spread distinct, but still closely related, variants of the virus to other parts of Africa and finally to the rest of the world. These distinct variants could then act as seeds (founders) for what later became classified as the different subtypes. The recent discovery of previously uncharacterized M group sequences in Central Africa lends considerable support to the natural origin hypothesis (Vidal et al. 2000) with a synchronizing local outbreak.

    IOW, the very possibility the other paper [the one this paper of yours was supposed to counter] investigated more deeply and found to be well supported.

    Satisfied?

    Again, to be clear, you accept that the cut hunters are proposing a massive iatrogenic “aggravating” event circa 1960, right?

    No.
    Scientists who study the issue have been looking into the ways known social factors that influence HIV propogation waxed and waned throughout the whole period. The needle re-use is pretty horrific, but it’s only one of many factors, and nothing started suddenly in 1960 or anything. It was a continuous process.

    Again, it is their job when many of those papers are explicitly claiming this as disproof of OPV, and it’s explicitly the job of the scientists outside of the paper to consider this possibility when citing these papers as disproof of OPV. What you’re saying here is nonsense. These scientists were behaving grossly incompetently or dishonestly when they were using the earlier dating papers as disproof of OPV.

    No, they were right.

    Hooper doesn’t like it, but that doesn’t make 2+2=5.

    I still completely unsatisfied by the dismissal of my argument that someone would have noticed the thousand HIV infected individuals before 1960.

    Tough.

    I’m not satisfied with the way Hooper is starting to preemptively poison the well about potential future retrospective cases early than 1957 by dropping hints that “conspirators” might fake the provenance of specimens. This is positively Trumpian. (What conspirators, even? The supposed conspiracy was 80 years ago, and pretty much everyone is dead at this point.)

  179. GerrardOfTitanServer says

    There’s obviously some overlapping, but 7000 samples still represents an awful lot of sampled chimps.

    Chimps are infamously territorial. You could have a million fecal samples, but if they all come from the same small number of sites, then you’re not really sampling that many individual chimps.

    Satisfied?

    I am an idiot.

    One further question: I’m still looking at the phylogenetic trees. Regarding the multiple-founders idea: It seems like the idea is a mass of virus strains in a small population with lots of mixing to obscure any origins behind that, and then you sample 10~viruses at random, and have each selected strain infect a separate population. Sure. That part makes sense. Under these assumptions, any two viruses from the original selection could be equally distant. I don’t completely buy it, but I’ll buy it for now.

    My question is: Where did that original soup of viruses go? It seems like this hypothesis only makes sense under the assumption that we had a small isolated population of incredible variety where 10~viruses leaked out of it to start the outbreak. This implies that we must have had a small but sizeable population of humans with the population of viruses with lots of internal spread to produce the initial conditions. My question is: Where did that original population of humans go? I guess we’re back to assuming some isolated group in some rural area, right? Ok. Do I have this all correctly understood?

    That means I was wrong. It does mean that we still have to suggest a highly unlikely history where we had an isolated population with lots of mixing that managed to survive for long enough to produce the initial conditions, and release all of the 10~strains to the wider world at just the same time, and then die off so that the great original variety of virus strains would not be detected. If it was a couple strains, I could believe it. If it was 8 strains, with 1 strain earlier or later, I could believe it. But it’s 10 strains at the same time to each of 10 different human populations. That still strains credulity. It also still strains credulity that no one would have noticed.

    Again, do I have a correct understanding of the process being proposed? I know we disagree about the plausibility of that process, that history. I just want to make sure that we’re agreeing on the proposed history.

    It was a continuous process.

    I thought the cut hunter modeling paper said that they had to assume a discontinuous jump in mutation rate of 3x at 1960 in their model for it to fit the data. So, in the real world it was a continuous process, but not in their models.

    No, they were right.

    Being right by accident is not being right in my book. I can’t believe you’re seriously advancing this argument. If someone is right because of a flawed argument, they were still wrong. They got to the right answer, but it’s just luck that they did. Ex: You score closer to 0 than 100% on a math test with all right answers but with wrong work shown in each case.

    What they did was clearly motivated reasoning because they didn’t like the conclusion. They’ve cleaned up their work since then, and kudos to them, but that doesn’t erase the original gross errors. It doesn’t remove the sin of extreme bias at the start clouding their original pronouncements.

  180. GerrardOfTitanServer says

    PS:
    And the recent cut hunter paper says that the “small, isolated tribe” was the biggest city in the Congo, Kinshasa, from 1920 to 1960.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4254776/

    So, if there was a great original variety of viruses that allowed for the multiple founder pattern, where did that great original variety go? There was an isolated group of humans in Kinshasa for 40 years?

    Or am I wrong, and the original variety of HIV in Kinshasa was no more and no less than the 10 separate strains which spread to the world, but my understanding is that this is not compatible with the multiple-founder hypothesis because we need a larger variety of strains from the origin-population to explain how the multiple-founder strains could be equidistant.

    So, again, where did this great original variety go? It was in Kinshasa for 40 years, supposedly, and then all disappeared practically overnight, leaving only the M group 10 founder strains that we know about today.

    Sorry, as soon as you try to put the story in the real world, it just doesn’t make sense. I’ll sooner sacrifice my belief in their novel dating techniques which AFAIK are not firmly grounded in real historical data, than I will sacrifice my understanding of the human history involved.

  181. jack lecou says

    Chimps are infamously territorial. You could have a million fecal samples, but if they all come from the same small number of sites, then you’re not really sampling that many individual chimps.

    You can check the papers. In the one I linked to, there were 567 individuals in 2500 samples. You’d have to click through to all of the source papers in D’s link to check those, but if a similar ratio holds, it should be at least 1600 or so.

    My question is: Where did that original soup of viruses go?

    They’re still there. Undifferentiated in Congo. Read. The. Papers.

    I thought the cut hunter modeling paper said that they had to assume a discontinuous jump in mutation rate of 3x at 1960 in their model for it to fit the data. So, in the real world it was a continuous process, but not in their models.

    Yes. The models are an approximation. It doesn’t actually mean there was a sudden “event” in 1960, just that on average things were happening where all these underlying factors were tending to accelerate around that time. We can imagine what’s going on underneath as something like a little bit of increase in activity in, say, 1954 in some areas, because of whatever factors, and then a little more in 1957 in other areas, and then in 1961 it builds up more back in the first areas, compounding, and so forth.

    Being right by accident is not being right in my book.

    They were not right “by accident”. They were right because they followed the evidence, made an approximation based on the best information they had, and did a pretty good job. Still more than good enough to trouble Hooper’s claims.

    You’re being confused because there has been some acknowledgement that recombination turned out to be “more important than first thought”. But “more important than first thought” is not actually the same as “completely falsifies early estimates”. The early estimates are still sound enough, so far as they go. And certainly at the time they were the best science available. Nobody was lying.

  182. jack lecou says

    Undifferentiated in Congo.

    I should say, less differentiated in the former Belgian Congo, and then even less differentiated than that in Kinshasa.

    Exactly what you’d expect from radiative spread, IOW. From Kinshasa to elsewhere in Congo, thence to the world.

  183. says

    jack lecou @ #s 185 and 186 and D @ #187, thank you for that information. I had questioned the titer-loss and temperature claims @ #151, but didn’t have anything to go on.

    There’s plenty of evidence that they amplified vaccine in Congo because that’s what Koprowski et al did when it was administrated in every other country, and because that’s what all of the other OPV groups were doing at the time. They had to. Even on ice, the vaccine lost titre very quickly, in a matter of days.

    It’s all so…roundabout. Hooper’s “evidence” that they amplified the vaccine in Congo is that they amplified it in these other places. His “evidence” that they amplified it in all of these places – despite not themselves indicating at the time or since that they did so – is that they must have, based on his assumptions and calculations about concentrations, titer loss, economics, competition,…

    His note #107 from that piece is interesting:

    In Africa, the problem was rather that of keeping the vaccine temperature below 4 degrees centigrade. Above this temperature, live poliovirus rapidly becomes inactivated. This was always the major headache involved in moving live vaccines, like CHAT, long distances around the world, and then out into the field. In reality, quite a lot of the live polio vaccine fed in places like South America, and the Congo, may have been useless, having fallen to a non-immunogenic titre because it got too warm.

    This actually would appear to undercut his larger argument, since the only “evidence” in its support is his insistence that they had to have amplified the vaccine locally due to titer loss. This note suggests that they were either unaware of or unconcerned about this alleged titer loss, to the point that “quite a lot” of the vaccine given in these regions might have been useless. It really only makes sense as a sort of smear, which he’s compelled to include even at the expense of his own argument.

    No. This isn’t a hypothesis that is merely pining for the fjords. It is no more. It has ceased to be. It is bereft of life. It rests in peace. It is an ex-hypothesis.

    :)

  184. jack lecou says

    It really only makes sense as a sort of smear, which he’s compelled to include even at the expense of his own argument.

    It’s weird, isn’t it?

    It also only makes sense if you suppose that even ordinary ice is entirely unavailable, let alone dry ice or liquid nitrogen. I feel like there’s a recurring tendency to treat 1950s Congo as if it’s 1850s Congo — at least when it’s convenient. At other times, of course, there is necessarily a fully equipped laboratory in the back corner of Congo, every bit as capable of making state-of-the-art vaccine as the main lab in Philadelphia.

  185. jack lecou says

    It really only makes sense as a sort of smear, which he’s compelled to include even at the expense of his own argument.

    It’s weird, isn’t it?

    It also only makes sense if you suppose that even ordinary ice is entirely unavailable, let alone dry ice or liquid nitrogen. I feel like there’s a recurring tendency to treat 1950s Congo as if it’s 1850s Congo — at least when it’s convenient. At other times, of course, there is necessarily a fully equipped laboratory in the back corner of Congo, every bit as capable of making state-of-the-art vaccine as the main lab in Philadelphia.

  186. GerrardOfTitanServer says

    My question is: Where did that original soup of viruses go?

    They’re still there. Undifferentiated in Congo. Read. The. Papers.

    I think you misunderstand me. Let me try again.

    Let me describe multiple founder effect – just to make sure that I understand it correctly. It goes like this: You have a normal population which can be explained by normal evolutionary proceses. This original population genetic tree doesn’t look like a multiple founder event. From this normal population, you take a few individual and move them to a new area and start a new second population. The genetic tree of that new second population would look very unusual. The genetic tree would look like a multiple-founder event with several strains that appear to have equal pairwise genetic distance. However, the genetic tree of the whole population (ancestor plus new) would look normal. It wouldn’t look like a multiple-founder event.

    The original problem is that the current HIV genetic data cannot be explained by normal evolutionary processes. So, some people proposed an ad hoc explanation – a multiple founder event. A multiple founder effect can explain the current data.

    However, that leads to the next problem. A multiple founder effect can explain the current data, but that entails that there is an ancestor HIV population out there whose descendants have not yet been sampled (except for the original 10 concurrent multiple founders). Again, if we had more samples of descendants of that original population (apart from the 10 original concurrent multiple founders), then we wouldn’t have the first problem of a highly unusual genetic tree. So, some people proposed another ad hoc explanation – the original ancestor population of HIV from circa 1920 to 1960 was in an isolated human population which either died out by present day before it and its human descendants could be tested, or the ancestor isolated human population and descendants still exist to this day in a state of extreme isolation and without any genetic testing. Fine – that fits the data.

    However, this leads to the next problem. That one cut-hunter proponent paper says that the HIV outbreak from 1920 to 1960 was centered in Kinshasa, the most populous city of Congo. This would mean thousands of human infectees circa 1960. Cut-hunter propenents try to ameliorate it by adding ad hoc explanation: the evolutionary rate of HIV was much slower in the past and drastically increased around 1960. With this third ad hoc explanation, the number of human infectees before 1960 in the Kinshasa area is lessened, but it’s still hundreds, maybe a thousand. The second ad hoc explanation of an isolated human population is simply inconsistent with data driven conclusion that the infection from 1920 to 1960 was centered in Kinshasa. Kinshasa is the exact opposite of an isolated human population. That’s a problem.

    So, under the assumption that the cut-hunter paper is right that the center of the epidemic from 1920 to 1960 was Kinshasa, the only remaining method that we can get a multiple founder event is if there was a severe bottleneck on HIV population survival which occurred circa 1960. This then leads to the obvious questions: What would cause such an extreme bottleneck on HIV population survival in 1960 Kinshasa? And for whatever answer you give, how is that compatible with the cut-hunter ad hoc hypothesis that at approximately the same time of this massive HIV population bottleneck, HIV was also experiencing a drastic increase in mutation rates and infectee population numbers?

    I’m sorry. This story doesn’t make sense to me. Not all of their data driven conclusions plus ad hoc explanations can all be true at the same time.

    PS:
    The simple answer appears to be to drop the assumption / conclusion that Kinshasa from 1920 to 1960 was the center of the HIV epidemic. I need to read the cut-hunter paper a few more times to understand why they seem so firm in that conclusion. I’m also surprised that they don’t see this obvious problem that I pointed out (Kinshasa is the exact opposite of an isolated human ancestor population which would be required for a plausible multiple founder effect).

    Even without the assumption / conclusion that the epidemic center from 1920 to 1960 was Kinshasa, even with the ad hoc assumption of a much reduced mutation rate before 1960, that still means about a thousand infected persons existing before 1960 in Congo, and again I say it’s simply not plausible that they escaped the retrospective notice of the medical community.

    And I still think that 10 multiple founders is extremely ad hoc. Has there ever been such a thing observed before? 2, 3, 5, sure, but 10? Possible, but extremely unlikely.

    Overall, that’s a lot of unlikely and extremely unlikely ad hoc assumptions to fit the data to the cut hunter model.

    By contrast, CHAT OPV hypothesis fits the data pretty well. The only assumptions that it has to make are: a small number of scientists involved in the original accident lied, plus a few more scientists circled the wagons, plus a few more scientists published ungrounded theoretical papers on novel dating approaches for RNA lentivirus (novel because HIV changes more by recombination than mutation compared to almost everything else by quite a wide margin) (and other scientists published papers that pushed back on the reliability of these papers).

    PPS:
    It’s completely mystifying that so many people here are taking the words of a few scientists in a few published papers as authoritative unchallengable fact. We should all know that like half of peer reviewed papers are shit. Scientific consensus emerges slowly over time, and that’s where the true reliability of science comes from. Scientific reliability cannot be found in a small number of cutting edge papers by the same authors.

  187. jack lecou says

    From this normal population, you take a few individual and move them to a new area and start a new second population. The genetic tree of that new second population would look very unusual. The genetic tree would look like a multiple-founder event with several strains that appear to have equal pairwise genetic distance. However, the genetic tree of the whole population (ancestor plus new) would look normal. It wouldn’t look like a multiple-founder event.

    Yes, this “normal population” is centered in Kinshasa, radiating out along lines of common travel to elsewhere in Congo and central Africa. It is still there.

    IOW, there are actually more than the usual 10 ‘official’ subtypes there (this is what “your” paper was talking about when it mentioned “previously uncharacterized M group sequences in Central Africa”), and they blur together, to the point where identification with particular strains is a bit murky.

    For example, a “D” subtype from, say, South Africa or Pittsburgh can normally be very clearly identified as such.

    But in Kinshasa, while cases might still be nominally identified as a particular official strain, when you look closely, you might say something like, “well, I guess I’d call that type D, but it could almost be a C, and there’s a little bit of E in there too, and I don’t even know what this is over here…”

    The actual distribution of HIV diversity doesn’t match an OPV “simultaneous origin” hypothesis at all.

    I think this obviates the rest of your questions.

  188. GerrardOfTitanServer says

    Jack
    Well. Thanks for getting to the crux of it. It’s my current understanding that your most recent post is very wrong. I’ll have to go re-read the papers again before I say more.

  189. says

    jack lecou @ 8 June 2021 at 5:04 pm
    I have to disagree with part of your characterization.

    But in Kinshasa, while cases might still be nominally identified as a particular official strain, when you look closely, you might say something like, “well, I guess I’d call that type D, but it could almost be a C, and there’s a little bit of E in there too, and I don’t even know what this is over here…”

    Rather I’d say the diversity in Kinshasa is basal relative to the official subtypes. So while certain Kinshasa sequences may be grouped with a subtype, as the non-Kinshasa sequences are a branching off from a Kinshasa lineage (founder effect, with the basal Kinshasa lineage then diversified independently of the geographically separated branches), other Kinshasa sequences are more basal and have similar distances to more than one subtypes.

  190. jack lecou says

    @202:

    Fair. I was trying trying to make that description brutally simple and concrete, but the accuracy definitely suffered. I think the upshot is the same.

  191. GerrardOfTitanServer says

    other Kinshasa sequences are more basal and have similar distances to more than one subtypes.

    Could you share a source that talks about that? That would be great. Please. Thanks.

  192. jack lecou says

    D might have something else, but AFAICT this one from up thread is probably the best round up that I’ve seen — so far, anyway.

    You can follow their references to some of the earlier genetic surveys and discussion if you like, which might more directly go to your question, but the analysis and visualizations in that paper itself are probably your best chance to understand what it all actually means. They’re doing a lot of work there to pull together all the available sequences and so forth and then do the statistics to figure out what that data can safely be said to be saying.

  193. says

    Indeed, that was the paper I understood to be under discussion. There are others, previous and more recent, that come to similar conclusions based on phylogony, but I don’t think they’d add much here.

  194. says

    Gerrard @ #199:

    PPS:
    It’s completely mystifying that so many people here are taking the words of a few scientists in a few published papers as authoritative unchallengable fact. We should all know that like half of peer reviewed papers are shit. Scientific consensus emerges slowly over time, and that’s where the true reliability of science comes from. Scientific reliability cannot be found in a small number of cutting edge papers by the same authors.

    This is super cranky. Also, you said to me @ #148 that Hooper’s “book ‘The River’ has over a hundred pages of references and footnotes.” This obviously proves nothing, since quality and not quantity is what matters; and I read some of his footnotes and found them wanting. Anyway, you’re arguing for the limited value of published papers while trying to support your case with a large number of references and footnotes. I assume you see the problem here.

  195. John Morales says

    SC, heh. No problem for Gerrard.

    Since it’s quality and not quantity that matters, it is meet Gerrard bookmarks and features the ones he figures advance his case, and dismisses the rest, though they are the bulk.

  196. GerrardOfTitanServer says

    Jack and D
    I have one more honest specific question. Are you saying that, in Congo, today and historically, we have found and sequenced HIV viruses that are clearly part of the M group but which also clearly fall outside of the known M group subtypes? If so, then I was sorely mistaken about one substantial point. If not, then I think my earlier point stands. If all of the known M group sequences fit nicely into one of the known 10~ M group subtypes, even if basal to one of the 10~ subtypes, this seems to imply a peculiar multiple founder event where the ancestor population has not been sequenced (apart from the 10 specific multiple founder strains). In other words, if the ancestor population had been sequenced, then we would have found other strains that are clearly part of the M group and also clearly not part of one of the 10~ M group subtypes (and not clearly a recombinant form). The idea that the ancestor population has not been sequenced (part from the descendants of the 10~ known M group subtypes) seems to be fundamentally incompatible with the idea that the ancestor population existed in Kinshasa / Leopoldville from circa 1920 to 1960.

    That is what I still don’t understand.

  197. Tethys says

    IANAG but the paper is not saying that the ancestor population has not been sequenced. As you might expect from the term recombinant, it breaks the known strains into categories. That does not imply that there aren’t other strains in the original location as they of course have evolved since jumping into human populations.

    Claiming that the paper is wrong because you don’t understand a fundamental feature of recombinant DNA is rather akin to someone asking ” If the Pilgrims came from England, why are there still people in England?

    Or, If humans evolved from Chimps, why are there still Chimps?

    It is my understanding that in the field of DNA sequencing,
    If the descendants have been sequenced, you in effect have also sequenced the ancestors.

  198. jack lecou says

    Are you saying that, in Congo, today and historically, we have found and sequenced HIV viruses that are clearly part of the M group but which also clearly fall outside of the known M group subtypes?

    That is exactly my understanding, yes. And not only that:

    If we imagine that sequences within one of the 9 or 10 usual subtypes are defined by having a genetic relationship to one another that’s analogous to the viral equivalent of siblings, or maybe 1st cousins*, then in Kinshasa (and to a decreasing degree, nearby locations in the CB), not only do we find ‘ordinary’ subtype members, we also — uniquely — find a bunch of sequences that:
    - don’t fall within any of the 9 or 10 common subtypes (are more like long lost 4th cousins to a member of one of those subtypes)
    - are equally related to more than one subtype (3rd cousins)
    - fall into an existing subtype, sorta, but not as closely as you’d normally expect (2nd cousins)

    So there are sequences that clearly fall outside known subtypes, yes, and sequences that fall inside, and also everything in between. Kinshasa uniquely exhibits the full spectrum of diversity that you’d expect to find in an ‘ancestor population’**, one that wasn’t fractured into genetically limited sub-populations by founder events.

    In fact, in some ways the diversity in Kinshasa kind of obviates the usual subtype classification altogether. If I understand correctly, the ‘normal’ subtypes are themselves the result of a clustering analysis. But when the same procedure is done on sequences from Kinshasa, you not only get more than the usual number of clusters, but the ones you do get are much less ‘clustery’, with a greater average distance between members. Again, as you’d expect in a “source pool”.

    So all the molecular data points to Kinshasa as the proximate source, with type M spreading from there first to elsewhere in the CB and then the rest of Africa and the world.

    What’s more, analyzing that data in detail can even show a lot of interesting stuff about when and where different branches radiated out. Which is precisely what that paper is doing. Contrary to Hooper’s very silly spin attempts, those charts aren’t just speculation, or some kind of ad hoc invention. The results come straight from the data (sequences and collection locations). (And you can check the error distributions — AFAICT, there really isn’t any statistical room for a simultaneous origin scenario.)

    -—–
    * Obviously the analogy to cousin relationships isn’t quite technically accurate for viruses (or, to the extent it is, it’s probably not 4th cousins, but 40th cousins, or 40,000th), but I believe that is roughly the gist. Certainly, even if that analogy isn’t quite right, the point is that the kind of type M diversity seen in Kinshasa is unprecedented.

    ** From the way you’re writing, I can’t quite tell whether you already know this, but note that it will obviously be impossible to ever sequence any actual “ancestor population”. The actual ancestors haven’t existed for almost a century, and with the exception of some early preserved specimens like ZR59, any sequences we have will necessarily have been taken from viruses that were living in at least the 80s, if not later. There were no living “ancestor populations” at that point, just descended populations with various degrees of Nth-level cousin relationships. The viruses in and around Kinshasa aren’t the ancestors, but the ancestors’ long lost heirs.

    If so, then I was sorely mistaken about one substantial point.

    If your source is Hooper, I think that would explain your confusion. It looks like Hooper has been in increasingly desperate denial about the state of the molecular data and what it says, going on about 20 years.

  199. GerrardOfTitanServer says

    That is exactly my understanding, yes.

    If so, then I was very wrong. If so, my confidence in CHAT OPV has dropped a lot. I would be no longer confident as asserting it as likely true. However, I’d still assert it as plausible.

    Still, this doesn’t match my understanding of the current HIV sequencing. However, I can’t find a clear answer either way.

    Thanks kind sir or maam.

  200. KG says

    Also:
    Coronavirus research is usually done in mere BSL-2 and BSL-3 labs. BSL-4 is for Ebola and stuff.

    And there are ~50 or more BSL-3 labs in China, sprinkled all over the country. There’s even another BSL-4, in Harbin. And probably hundreds of BSL-2s. I’m not sure there’s any city in China where an outbreak could start and you wouldn’t be able to find a lab across town or just up the road somewhere that’s potentially doing coronavirus research. It’s just really not as much of a coincidence as you might think. – jack lecou@83

    Sorry to come back to this after a longish gap, but just looking through this thread after a longish absence (after noticing a stream of comments from GerrardOfConspiracyTheories), I saw your comment. First, the current pandemic (following the outbreaks of SARS and MERS) surely indicates that bat coronavirus research should only be carried out in labs with the highest level of security. Covid-19 has killed a lot more people than ebola or even, in the last half-century, smallpox.

    Second, your comment prompted me to do a Scopus search on “bat coronavirus China” for the period 2010-2019. The only other city in China with research activity on bat coronavirues at all comparable to Wuhan appears to be Hong Kong (Beijing has some, but authors of bat coronavirus papers with an affiliation “Chinese Academy of Sciences University Beijing” generally have another affiliation, usually to Wuhan Institute of Virology, I found no articles without an author with an affiliation from at least one of Wuhan, Hong Kong or Beijing). Most of the articles I looked at which involved actual sampling from bats (around 30) were sampling from places in Yunnan, but of those 10 with authors at Yunnan Institute of Endemic Diseases Control and Prevention all but two had first authors from WIV. It’s quite clear WIV is the major centre for research on bat coronaviruses in China, University of Hong Kong being the only place that even runs it close, while Yunnan has been the main area in China studied by researchers on these viruses, primarily by researchers from WIV. Presumably if they could collect such viruses from Hubei or nearby provinces, they would do so.

  201. jack lecou says

    First, the current pandemic (following the outbreaks of SARS and MERS) surely indicates that bat coronavirus research should only be carried out in labs with the highest level of security. Covid-19 has killed a lot more people than ebola or even, in the last half-century, smallpox.

    AFAIK, biosafety levels have very little to do with how deadly a virus potentially is. Rather, the idea is to specify equipment and safety procedures that are appropriate to a specific virus’ properties (does it spread via fluid contact? blood? sweat? is it airborne?) as well as the nature of the experiment (pipetting virus suspended in fluid would usually be inherently safer than, say, handling infected lab animals).

    Everything we know about SARS-CoV-2 says that if properly followed, relatively lightweight safety measures like gloves and a filter mask are more than sufficient. Which is, IIRC, roughly BSL-3. And for certain work, one can see how even BSL-2 would be sufficient.

    By contrast, BSL-4 is full positive-pressure rubber suit, sealed room type stuff. That makes sense with Ebola, which spreads via basically all the vectors, but it is almost certainly overkill for CoV. Even deadly strains like SARS. Just making everything BSL-4 won’t necessarily make anything safer. A higher level comes with complications and costs, and possibly different kinds of risks, like compliance. It is actually important to pick the right one.

    Which isn’t to say there isn’t room for improvement. I think the tricky part is in the “if properly followed” qualification. BSL-3 is probably the right level for CoV, but it needs to be the best BSL-3 it can be. We need to make sure that the guidelines — at every biosafety level — are actually comprehensive and don’t have any holes, and then that those protocols are really being followed correctly when put into practice, even at lower profile labs, that accidents are properly detected and reported, etc.

    It’s quite clear WIV is the major centre for research on bat coronaviruses in China, University of Hong Kong being the only place that even runs it close, while Yunnan has been the main area in China studied by researchers on these viruses, primarily by researchers from WIV. Presumably if they could collect such viruses from Hubei or nearby provinces, they would do so.

    Yes, WIV is certainly a big one for CoV stuff, at least in English language/international science publications. That doesn’t necessarily mean there aren’t other labs working on non-published stuff, sample or data collection ultimately destined for WIV, etc.

    But also, that’s not really the point. I said potentially, because I don’t think it actually matters to the conspiracy theorists what public information says a lab is or isn’t working on. Remember that early conspiracies — and a lot of them are probably still at it — weren’t actually even talking about the WIV. They were conspirating about an entirely different lab in Wuhan, a smaller one, associated with the Chinese CDC, that’s apparently attached to a clinic a couple of blocks from the infamous “wet market”. It’s not clear that one works with bat samples at all, but it doesn’t really matter, does it?

    Presumably if they could collect such viruses from Hubei or nearby provinces, they would do so.

    Well, they certainly have in the past. In the early 2000s I believe there were more known CoV samples from Hubei than from Yunnan.

    It’s really just an issue with small sample size. AFAICT, the total level of bat CoV surveillance, compared to the actual number of bats out there and their geographic range, is a drop in the ocean. Whether it’s a funding issue, or just the sheer difficulty of the work, only a tiny, and not necessarily representative, fraction of bat populations have been sampled.

    From what little I’ve read, I got the impression that WIV has been sampling heavily in Yunnan for the past few years not because those are the only bats in China, or the only ones carrying CoVs, but rather because it’s low hanging fruit. There are a couple of caves and mines there where collection is relatively tractable, and interesting viruses are found regularly. It’s possible they’ve been neglecting other areas that are a bit more difficult because Yunnan was already providing plenty of research possibilities.

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