Michael Egnor agrees with me, I’m having a panic attack


Uh-oh. Michael Egnor is writing about me over on the Discovery Institute site. He’s commenting on that summary of the origin of SARS-CoV-2 virus I wrote the other day, which is fine. What isn’t fine is that he agrees with it.

I threw up in my mouth a little bit.

Reading further, though, he agrees with it for all the wrong reasons, so I feel a little better.

Myers, like the Nature Medicine scientists, uses the scientific inference to intelligent design to search for (and discount) human intelligent agency. Design science is at the forefront of research on the emergence of coronavirus. Based on the available evidence and using the inference to design as a scientific hypothesis, intelligent design of the COVID-19 virus seems unlikely.

That is incorrect. “Design science” is not at the forefront of the research. The authors of that paper came to their conclusion by extensive comparisons of the viral sequence with viruses in other organisms, and by a functional analysis of the structure of the receptor binding domain. Conspiracy theorists and creationists have been poisoning the global conversation with nonsense about the virus being “designed”, so they addressed and dismissed that idea. The primary interest was in the original source, and what properties of the virus make it dangerous to us.

They also pointed out two major adaptations of the virus spike protein: changes to the receptor binding to allow it to bind effectively (but not optimally) to the human ACE2 protein, and an insertion that adds a polybasic cleavage site which also allows the linkage of glycans to the protein that assist in immunoevasion. Two mutations at once! Doesn’t his pal Michael Behe have something to say about the improbability of multiple mutations?

But there is another lesson about design and evolution to be learned from scientific research on this virus. Natural selection, if understood as undirected variation and differential reproductive success, is a destructive process. Natural selection destroys biological functional complexity — it produces diseases, cancer, and pandemics. It weakens and kills. Natural selection does to living organisms what rust does to a machine. Natural selection corrodes and destroys life, and plays no role in creating it.

Not for the virus, it wasn’t a destructive process. What was undergoing natural selection here was the virus, not us, and it has acquired attributes that make it wildly successful — it is now colonizing vast fields of billions of human beings, producing uncountable numbers of progeny, infecting more people at an accelerating rate. The virus is stronger and thriving thanks to those features, and doing very well thank you very much.

Humans are now possibly undergoing a round of natural selection in response. I don’t know if there’s a pool of heritable resistance to the virus in the population, so it’s possible we’re experiencing a field of bullets scenario, where nothing heritable is being selected for, but if there is a genotype that has an advantage here, natural selection would increase their frequency over time. Natural selection could make us more resistant as a species to SARS-CoV-2, and definitely wouldn’t be a destructive process.

Also, one of the features of the virus is the addition of short sequences, so SARS-CoV-2 may have had a slight increase in complexity over its predecessors.

Egnor is basically wrong about everything. Balance is restored to the universe.

Comments

  1. raven says

    Design science is at the forefront of research on the emergence of coronavirus.

    There is no such thing as Design science.

    Natural selection, if understood as undirected variation and differential reproductive success, is a destructive process.

    This is completely false.

    It’s a repeat of the creationist lie that evolution can’t result in beneficial mutations.
    This is empirically wrong.
    Natural selection can and does frequently produce beneficial mutations every where we look.

    The end result from single celled prokaryotic ancestors is a vast amount of complexity. We call it the biosphere and part of it is us.

  2. raven says

    It’s ironic that a lot of people who don’t believe in evolution are going to get sick and some will be killed by, a newly evolved viral disease called Covid-19.
    Reality and viruses don’t care what you believe.

    It’s also ironic that fundie xians will most likely die of Covid-19 in higher numbers than the general population.
    This is what happened during the Swine Flu pandemic of 2009.
    They claim to have an invisible Sky Monster god who protects them.
    The fact is, their invisible friend doesn’t actually do anything.

    Reality and viruses don’t care about your invisible friend either.

  3. euclide says

    Since the virus is mainly killing older (and above reproduction age) people, won’t the evolutionary change on the humanity side be limited ?
    As opposed as the spanich flu, which killed a lot of young aldults

  4. Artor says

    Euclide, your data is a little past date. The Orange Death is dropping people of all ages, not just older victims.
    A friend of mine, who sadly lacks effective bullshit filters, was telling me breathlessly yesterday all about how the coronavirus was patented back in 2014. I had to explain to him that the coronavirus was a whole family of viruses, some of which have been used in research for years. I don’t know where he got his erroneous information, but he’s someone who watches the History Channel and assumes everything on there is actually history. It’s right there in the name!

  5. azpaul3 says

    But, GOD designed the virus. It is punishment for opposing his chosen one, Trump. And because of the Jews or the Muslims or the gays or the feminists or the liberals or …

  6. says

    Yeah, the virus is killing people of all ages. Also, don’t you know about the Grandmother Hypothesis, that older generations make a significant contribution to the welfare of their grandchildren? My wife is off practicing that principle right now, although one could argue that I have passed the age of usefulness.

  7. raven says

    Bloomberg.com
    Many New York Coronavirus Patients Are Young, Surprising Doctors

    New York has more confirmed cases than anywhere else in the U.S., and about 1 in 5 hospitalizations are occurring in people under age 44, according to data released by the city’s health department.

    The Covid-19 virus is already known to seriously infect younger people.
    With hospitals overfilled, you don’t end up there unless you are very sick.
    While younger people are more likely to survive, they can and do end up with permanent lung damage.

    NBC.com

    According to the South China Morning Post, doctors at Hong Kong’s Hospital Authority have noted some (20-30%) of COVID-19 patients experience drops of 20 to 30 percent in lung function. Other studies have hinted that COVID-19 infection could lead to heart injury, which is damage that can occur when blood flow to the heart is reduced.

    A lot of those young people that survived Covid-19 pneumonia and being on a ventilator for weeks will have permanent lung damage that will effect them for the rest of their lives.

  8. wzrd1 says

    @3, the 1918 Spanish influenza pandemic is a poor example, as there is evidence that the elder population was more resistant to the virus due to a predecessor variant of that same virus from 1898.
    More importantly, PZ tried to hop onto the wrong boat with heritable changes to result in immunity to the virus. Look at an old and unwanted companion, malaria. People have shown some genetic changes that mitigate against infection, but at a cost, as the advantage of being less effective as a host is balanced by intolerance to some foods for one deficiency, defective hemoglobin that’s ineffective in another and hemoglobin that’s malformed but functional and results in red blood cells clogging capillaries in another, to name just three adaptations that are sub-optimal. In short, things need to stew longer to find a clear advantage that’ll outcompete in reproductive survival long term just for malaria. Now, look at influenza and the lack of most animals adaptation against the damnable virus!

    @4, perhaps your friend got that tidbit from Drunk History?

  9. unclefrogy says

    it is amazing, such a combination of ignorance and arrogance, can lead to looking at the simple truth and coming up with the wrong conclusions any way.
    uncle frogy

  10. wzrd1 says

    @12, a journal is not a field of science or study.

    Design Science is an international open access journal publishing original quantitative and qualitative research in the creation of artifacts and systems, and their embedding in our physical, virtual, psychological, economic, and social environment.
    Peer reviewed by an international editorial board, Design Science aims to serve as the archival venue of science-based design knowledge across multiple disciplines. The Journal will facilitate communication across diverse fields and will serve as a bridge across several communities, publishing original research with a strong emphasis on accessibility by scholars from a diversity of disciplines.

  11. raven says

    Hmm Raven, apparently Cambridge University would disagree with you about Design Science:

    No they wouldn’t.

    Like creation science, intelligent design centers on Paley’s religious argument from design, but while Paley’s natural theology was open to deistic design through God-given laws, intelligent design seeks scientific confirmation of repeated miraculous interventions in the history of life.
    Intelligent design – Wikipedia

    Religious creationist “science” isn’t science. It’s a cargo cult that uses the terminology and appearance of real science to prove the existence of the gods.

    There is another key difference between creationism and science.
    Intelligent design’s attempts to prove the existence of the gods has so far failed completely.
    Science, on the other hand, works and works well.
    It is a key foundation of our modern Hi Tech societies.

  12. davidc1 says

    The Doc @7 We will keep you around to fight all them barmpot RNJ’s ,stuffed and mounted if necessary .

  13. billseymour says

    Egnor:

    … intelligent design of the COVID-19 virus seems unlikely.

    LOL! Figured that out, did ya?

    My main takeaway from what little I know of science is how tremendously easy it is for us to delude ourselves. That’s why scientists ask the questions first and try to find the answer second. 8-)

  14. chrislawson says

    It’s pathetic. Egnor is trotting out stupid misrepresentations of Darwinian theory that were wrong in 1859. Maybe he should take up the cause of phlogiston next.

  15. chrislawson says

    yannouipouka–

    Your link is to Design Science, a journal dedicated to the scientific study of “the creation of artifacts and systems”. A journal name is not the same as a field of science (Cell, for instance, is not dedicated to the field of “cell science” and although communication is an actual scientific field, Nature Communications is not dedicated to it).

    More importantly, it is about the study of unambiguously human-designed systems and has nothing to do with Egnor’s “Design Science” which is a made-up term to describe his fellow anti-evolutionary know-nothings reinforcing each other’s fallacies without doing any investigative research and studiously ignoring, misrepresenting as supportive, or fake-rebutting other people’s research.

  16. notbuyingit says

    I’m part way through reading Behe’s “The Edge of Evolution”, but corona virus having 2 mutations doesn’t necessarily affect the arguments that he makes from mutations in malaria:
    1. Corona virus genome is pretty small. Wikipedia lists it as about 30,000 bases vs malaria at 28,000,000. The chances of getting 2 required mutations may be much larger in the smaller genome (i.e. chances of getting 2 consecutive numbers in sample of 30,000 is much better than in a sample of 28,000,000, i.e. 9×10^8 vs. 7.8×10^14)
    2. PZ says “Two mutations at once!”, but only gives evidence that there are 2 mutations. Two mutations can also arise sequentially (i.e. not “at once”), which Behe does not seem to have an issue with.
    3. Behe says that population size will be an important factor in improbable events. I’m not sure how many viral particles are produced in the average human infection, but I would think it could be large? (does anyone know how many infectable cells are in the lungs, and how many particles produced per cell?)

  17. strangerinastrangeland says

    “…intelligent design of the COVID-19 virus seems unlikely.”

    Hmm, doesn’t Mr Egnor and his chaps at Discovery believe that everything is designed intelligently by a god (sorry THE GOD)? And then Covid-19 is the only thing that evolved naturally? I am confused…

  18. says

    PZ says “Two mutations at once!”, but only gives evidence that there are 2 mutations. Two mutations can also arise sequentially (i.e. not “at once”), which Behe does not seem to have an issue with.

    Yes, exactly. Which makes Behe’s whole argument from the improbability of multiple mutations nonsensical.

  19. notbuyingit says

    The issue is that Behe himself makes the distinction between a scenario requiring 2 simultaneous mutations for any benefit versus a scenario requiring the same number of mutations but where the 1st mutation conferred an advantage without having to wait for the 2nd mutation. The 2nd mutation (after the 1st one is fixed in the population) then has the probability of a single mutation. Behe thinks the 2nd scenario is quite achievable; he thinks that the 1st scenario is much, much less achievable. The important point is that they are 2 different scenarios, with 2 different probabilities, and Behe is clear about this.

    Using the corona virus mutations above as an example, if (for arguments sake) the “binding” mutation occurred 1st, then this might give the virus the ability to jump to the new host (us!) and if so, then it’s next challenge would be to evade our immune system. But given that the entire population in the human host would now have the “binding” mutation (otherwise it wouldn’t be able to replicate), the virus would just have to stumble on the “evasion” mutation before antibodies were produced to destroy it. I’m not actually saying that this occurred, but just highlighting that if mutation 1 has a strong selective advantage (i.e. invading a new host) and becomes speedily fixed in the population, then mutation 2 becomes much more probable.

  20. chrislawson says

    notbuyingit–

    Just for your edification, I know a bit about viral loads in HIV and HepC, and one of the highest viral loads ever recorded for HIV was a Zimbabwean woman who had 1 058 239 000 copies/mm3 of blood. That’s a billion viral particles per ml. Since the replication time for HIV is about 1-2 days and the average blood volume in a person is 5L, that means that in she had more HIV replication events in an hour than the entirety of humans in our history.

    Good luck getting sense out of Behe. The entire premise of “necessary” mutations is wrong. Mutations are random. Behe likes to concentrate on a specific jackpot to calculate his probabilities, but in reality there are a near-infinite number of jackpots a mutation can hit. Behe likes to calculate (incorrectly) the odds of getting a bullseye and pretend it’s the odds of hitting the dartboard.

    And even then, we observe these positive mutations happening and being selected for. There is no question that advantageous mutations happen frequently enough to drive antibiotic resistance, pesticide resistance, and so on. Behe’s biggest dishonesty is that he provides a wrong estimate of probabilities and argues that since his wrong estimate doesn’t match reality, that proves that goddidit where an honest researcher would conclude that a better theory is needed.

  21. notbuyingit says

    chrislawson-
    Thanks for the info on HIV. I suppose that the number of corona viral particles would not be anywhere near that large, but my googling didn’t yield anything. I also had no luck in finding how many lung cell on average were infectable.

    As far as the “dart-board” analogy, Behe actually addresses this on p61 of his book. As he points out, due to the exceptionally large population size of malarial parasites in any given year, and the 6 decades or so that chloroquinine has been in use, we would expect that every combination of single and double mutations would have shown up in the malaria population in this time. Regardless, chloroquinine has been ruthlessly destroying the parasites unless they had the effective mutation pair – the bullseye. All of the other mutations are peppering the dart-board, from the edge of the dart-board all the way to just outside the bullseye, and still the malaria parasites die by the trillions because those mutations don’t lead to chloroquinine resistance.
    Behe isn’t just speculating here, he’s basing his conclusions on the evidence of a massive real-world experiment. He also gives examples of other drugs that required a single mutation to thwart, and resistance to these developed very quickly (sometimes even in the lab.) I also did a quick search to see if his “2 simultaneous mutations required” assertion holds water, and I found that a report in “PNAS” from 2014 confirmed this. The report also stated that further mutations could then increase the resistance, but that 2 was the minimum.

  22. chrislawson says

    Sorry, notbuyingit, but Behe is lying about that massive real-life experiment.

    From the CDC page on drug resistant malaria:

    “Chloroquine-resistant P. falciparum first developed independently in three to four areas in Southeast Asia, Oceania, and South America in the late 1950s and early 1960s. Since then, chloroquine resistance has spread to nearly all areas of the world where falciparum malaria is transmitted.”

    Not only has falciparum malaria evolved resistance to choloroquine, it has done so in 3-4 independent populations. And so has vivax malaria.

  23. notbuyingit says

    chrislawson-
    Behe actually mentions (p49) that multiple occurrences of resistance have evolved (his reference mentions 4 independent occurrences.) He is not saying that it can’t occur, just that the difficulty that malaria had in evolving the resistance gives us an indication that the 2 simultaneous mutations that were required were of a very low probability that required enormous population sizes of malaria parasites to overcome. He contrasts that with resistance to other drugs that only required a single mutation, and in those cases resistance developed in much shorter periods of time. He then references research (p57) that uses the time taken to evolve chloroquine resistance combined with estimates of the annual number of malaria parasites exposed to the drug, to come up with a figure of 1×10^20 as the probability of chloroquine resistance occurring.

    Again, Behe never said that chloroquine resistance had not arisen – it obviously has. His book is about drawing conclusions about the pace at which multiple simultaneous mutations can be expected to arise by random mutation. I’m only part-way through the book, so I’m unsure of what further (if any) arguments he will make.

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