Worrisome news from China:
A person who had close contact with a dead H7N9 bird flu patient in Shanghai has been under treatment in quarantine after developing symptoms of fever, running nose and throat itching, local authorities said late Thursday.
So far, China has confirmed 14 H7N9 cases — six in Shanghai, four in Jiangsu, three in Zhejiang and one in Anhui, in the first known human infections of the lesser-known strain. Of all, four died in Shanghai and one died in Zhejiang.
That first paragraph is the really scary one: it suggests that there may (emphasis on the possibility, it has not been demonstrated) have been human-to-human transmission, rather than just bird-to-human. The latter case is slightly more manageable — avoid ducks. The former case would require avoiding people — not so easy.
The H5N1 bird flu virus, different than this one, had about a 60% mortality rate, but 36% mortality for H7N9 so far is not good. Also, H5N1 was lethal to birds, too — this one seems to be relatively harmless to the bird carriers, while being relatively deadly to infected humans.
Where do I get the vaccine?
I’ve been following the various bird flu strains for some number of years now as part of my capacity as an educator of health care professionals. I create an annual lecture series on influenza for physicians and nurses.
In my opinion, it’s WAAAAAAAY too early to strike any gongs of alarm. Don’t start hoarding rice and beans and beef jerky just yet.
Not that it couldn’t happen. The movie “Contagion” is a pretty darned accurate assessment of a scenario that would involve a strain like H7N9 becoming more contagious while maintaining its lethality.
The combination of low mortality in the reservoir population with high mortality in humans is very worrying. Lets hope the human-human transmission is ineffective.
Possible human to human transmission would be a bad thing. I hope it turns out not to be the case and that this is all quickly controlled.
It’s all the gays’ fault, I’m sure.
What worries me most as a virologist is the fact the we can’t easily see it in avian hosts, unlike H5N1, which has this odd tendency to kill anything it infects. Not being able to track this one is very worrying. From my point of view, developing the capability for human-human transmission in birds is low, but if a human or pig was co-infected with H7N9 and a highly transmissible seasonal flu like the typical H3N2, H1N1, or 2009 Novel H1N1, a reassortment could occur that would give H7N9 the ability to move rapidly within a population of humans.
No One @1:
You don’t. There is no vaccine for H7N9.
There’s some thought that the strain may be vulnerable to antivirals, though.
Ragutis:
Nope. Rebecca Watson. Again.
Vaccine: Remember how long it took to make the H1N1 vaccine back in 2009? It’ll take nearly twice that to make one against H7N1, (due to various technical issues) and even if we make a vaccine in time, random mutations in the target epitope(s) could render the vaccine next to useless, or at least much less effective. Oseltamivir (Tamiflu) should still work though, if we have enough…
*H7N5. Damn you Tpyos!!!!!!
I always mix up H1N1 with the H-1B visa. Whoops. @A R, this might be a dumb question, but is that how it works? The H7N9 sort of piggy backs with a more contagions illness that you also have?
and
good bye sleep tonight. That movie still frightens the crap out of me.
What does the notation HxNy mean? The chemist in me wants to interpret it as some weird hydrogenated azide.
Well, it could be the transmission method was something really unlikely or just uncommon, like bodily fluids or somesuch.
*Hydrated azide
@Jacob Schmidt
It refers to variants of two surface proteins; hemagglutinin and neuraminidase; used to classify different strain of flu virus.
http://en.wikipedia.org/wiki/Influenza#Structure.2C_properties.2C_and_subtype_nomenclature
yazikus: No, but if you are infected with two flu viruses simultaneously, they can swap genome segments (Influenza viruses have octosegmented genomes, and they randomly assort when enteroing budding viruses (which means that most virions don’t receive a full genome (they can receive multiple copies of one segment, but none of another, etc.), and are therefore not infectious) so if two flu strains infect a cell at the same time, they can easily swap genes.), which can lead to a sort of hybrid virus (technically a reassortant virus) with characteristics of both of the strains that infected the cell. So you can see how you could get a virus with genes for virulence and transmissibility. We think that this is how many pandemic flu strains develop, and we have some pretty substantial evidence that this is how Novel 2009 H1N1 evolved.
Crissa: That’s what I’m hoping for. It’s damn easy to transmit something via blood or bodily fluids. Airborne or droplet transmission however…
The surface proteins are targets for drugs and antibodies, since they’re at the surface (duh) and therefore accessible. That’s why it makes sense to classify virus according to this system.
@A.R
Thanks for the explanation. That is pretty frightening, but makes sense.
AR, don’t you mean the other way around? Easy to transmit via air or droplets, harder by blood or other bodily fluids?
We’re damn lucky Canada’s boards of health jumped on SARS with both feet before it could get out of the barn.
Yeah, don’t panic. Small numbers so far, and the possible case of human:human transmission is only that, possible.
Don’t panic? Are you mad! As someone who’d have to shave off their beard in order to fit an N95 mask, I say panic.
Okay, I got my degrees in English and Philosophy, so I’m not sure what to make of this. Just break to me straight: should I be working on my Bucket List or not?
I wouldn’t be terribly worried until we have more than three confirmed cases of human to human transmission and we can establish an R-naught.
Markita Lynda, fluid to fluid transmission is easy for the virus, airborne harder to adapt for. Just about any virus can do bloodborne transmission. Fortunately it is a situation that is easier for multicellular organisms to avoid.
Airborne transmission required a hardier virus, and of course if it happens with a very nasty one, perhaps with both high latency and high lethality, well then we are screwed.
(According to memories of an interested amateur, take with a grain of salt unless confirmed by A.R or other pro.)
MFHeadcase! It’s good to see you around here again.
Chris Clarke
Plan B, nail the windows and doors shut.
okstop:
Color me stunned… a philosopher rendered speechless by a mere virus *.
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*meant in good fun.
Well that’s not good. I’m living n Zhejiang right now… And my housemates been sick… Here comes the paranoia.
For those of us who are not virologists and related professions, I strongly recommend John Barry’s The Great Influenza . This is an enormous book that starts off not with pigs in Nebraska (where they are pretty sure it started), but medical science education on the east coast a couple of decades earlier. It explains how and why medical science was so nearly helpless, how the politicians, especially the US President, shut their eyes, plugged their ears, and yelled “La la la la la I can’t hear you” with horrifying results. It talks about what the epidemic was like (focused almost entirely on the US–I suspect because of length issues). It explains why that particular virus was so deadly to healthy young people when it is the very young, sickly, and elderly who usually die of influenza.
It is a very well written book, though it does get a little melodramatic in spots. When you finish it you will have a better understanding what this whole influenza thing is about.
I’ve had influenza twice, both when I was in my 20s. It was bad. I am very careful about getting my shot every year, even though I know that doesn’t guarantee anything. I do not want to be that sick again now that I am nearly 63 with asthma.
And I hope that this version of H7N9 doesn’t get loose. It’s a lousy method of population control.
I try to avoid ducks, but sometimes ducks happen …
WHO has an FAQ on H7N9.
WHAT is with all the pop-up ads?
WHO is a fantastic resource for following this sort of thing.
I agree with AR — it’s not necessarily the current strain that’s a threat — but if there’s a reassortment (which happens a lot in swine that become co-infected with two different strains that then swap genetic material), then bad things could happen.
The 2009 H1N1 was a triple reassortment. That was one sick pig.
In all seriousness, I wonder if it is only a matter of time before some type of terrorist can easily develop a virus or biotoxin which will cause a pandemic. Its only a matter of time before we discover much of how the biochemistry of cells work at a fundamental level. I don’t think this threat is really considered deeply enough.
Or maybe it is and we just aren’t aware of the details.
Why would we be?
@ A R
if you’re still around:
Talking about viruses and transmissibility vs. virulence, etc. …
Do you know anything about Ebola/Marburg?
The existence of Ebola Reston scares me [I mean, when I think about it – I know that I don’t need to worry about it as any sort of immediate threat], but the filoviruses are constructed very differently from influenza – are they able to do a similar reassortment? It’s something I’ve wondered for a long time, but I don’t know any virology, so… I just have no idea what would be happening chemo/biologically that would make it possible for an Ebola Reston variant to [re?]acquire the lethality of Ebola Sudan. Also, I have no idea if the qualities that give it airborne transmissibility are incompatible with lethality, or just didn’t happen to co-occur this time, or something else more complex (like it affects lethality, but doesn’t prevent it if X other factor is present that does not affect transmissibility but negates the diminishment of lethality that the airborne transmissibility genes would otherwise cause).
Anyway, I’d happily read something about ebola instead of contract law. What the heck, my final isn’t til next friday.
Would it be possible (and not horrendously dangerous) to flood someone’s immune system with a wide spread of monoclonal antibodies?
I’m not a biologist of any sort, but you’d think that would be the immune-system equivalent of “sudo rm -f H*N*” or a similar regex-like targeting of flu viruses…
Big lesson learned from 2009: We can not produce enough vaccine doses fast enough to protect everyone.
If the super flu appears one day, we will only be able to slow him down a little with our current technology. After all, we still breed chicken eggs to make those vaccines.
People are also working on recombinant production of influenza vaccines. This could cut down the time between virus isolation and production of several hundred million doses to a month or maybe even less.
@ Crip
The consensus in the community is that we need to worry much more about flu than Ebola. Ebola might form a super bug, flu most certainly will. Like it did before.
I had no doubts that Influenza is the greater threat. I’m just curious b/c that reston thing was scary.
Crip Dike: I’m working off of my iPhone right now, but I’ll post about Ebola tomorrow. It’s my specialty by the way.
37,
The (unknown) carrier species for Ebola and other hemorrhagic fevers (some people say it is bats) seems to be confined to certain remote tropical areas. An outbreak is much easier to confine while flu tends to develop in densely populated areas close to airports and harbors. The fact that the carrier species is so hard to identify also tells us that the virus is not much prevalent in those pools.
I can not tell you if Ebola undergoes reassortment like flu does, if anyone could tell you, those viruses are little known and notoriously difficult to study, but I can re-insure you that the fact that those viruses are rare drastically reduces the likelihood for reassortment in a host cell since it becomes much MUCH less likely that two different viruses infect the same host cell the same time. So, if reassortment can occur in Ebola, it should be many magnitudes less productive then within flu.
I hope that helped.
Caine @26, I am often around, I lurk more than posting. **wry grin** I never thought my comment density was high enough to be missed.
MFHeadcase, it wasn’t comment density which caused you to be missed, but your comment quality. :)
Ugh, now I´m wondering what that person was doing with/to the dead patient.
lamaria @42, the simplest explanation is that they were a friend, family member, or even lover of the dead patient with the contact being before the potential seriousness of the disease was known. They could well have been asymptomatic until AFTER the previous patient was hospitalized.
They could also have been hospital staff, but someone who doesn’t normally come into contact with fluids. Thus the extra worry.
Or hell, even one of the crew that works corpse disposal who screwed up.
It doesn’t have to be nasty, just unlucky.
Or they could’ve had contact to the same source the patient did, or close enough to. We only know they were in close proximity for a time.
A lower mortality rate is not very comforting, especially if the avian carriers are not killed. They could instead survive to carry the new strain across borders and into new populations. Is there any info on how virulent this is compared to previous versions?
~:-| …No, you were right the first time: there’s H but no O, so hydrogenated, not hydrated.
@Crip Dyke re: ebola
Ebolaviruses are not capable of reassortment, as they have a one-piece genome. Mutations in ebolavirus genomes appear to occur at a rate much, much lower than what we see in Influenza, to the extent that a virus may change very little during the many passages it experiences during an epidemic. This genome stability may have something to do with the nature of the ebolavirus nucleoprotein (the protein portion of the nucleocapsid that binds to the genomic RNA). Regarding Reston virus, we aren’t incredibly sure why it doesn’t affect humans in the same way that it infects monkeys, but the prevailing theory relates to the function of VP30 (which has some anti-Interferon function), and the products of the GP gene, which are the components of the polymeric spike glycoprotein, a pair of secreted glycoproteins, and a small peptide. It is unlikely that Reston virus will mutate into a human-pathogenic form anytime soon, despite its antigenic similarities with Zaire ebolavirus. In addition, there is some evidence that the apparent airborne transmission of Reston virus was actually a result of reuse of needles by staff in the handling facility, as airborne transmission of then type suspected in that outbreak has not be replicated to my knowledge. Finally, the probability that an ebolavirus would develop the capacity for airborne transmission is relatively low, as there is no selective pressure for it, and outbreaks are so scarce, and major mutations rare enough that even if there was selective pressure, it would not necessarily result in a strain with airborne transmission.
patterson@22: as my old boss used to say: “It’s never too early to panic.”
@Azuma Hazuki #35:
Fewer greedy searches, please! Let’s just start off with ‘H\dN\d’, OK? With yours, my liver felt a bit better at first but then I wasn’t so sure about my blood pressure…
@49/Rich Woods
Oops, sorry. Maybe that should have been H.?N.? then? I’m still a little new to regex. You might say…a bit awk-ward *runs*
Azuma Hazuki: Actually, there is a way to do that. Several groups are working on developing an Influenza vaccine that would target highly conserved (that is, very similar between strains, and not likely to mutate) parts of the proteins. This really can’t happen naturally because these regions are typically fairly inaccessible to the B-cell (a type of white blood cell) receptors (which are actually antibodies bound ot the surface of the B-cells instead of floating free) that need to bind to them to stimulate the production of antibodies against them. To understand why this is, imagine hemagglutinin (the “H”) as a tree with a massive crown. The crown of the “tree” contains the places that B-cells typically recognize and produce antibodies against, but these places mutate rapidly, and are specific to one type of hemagglutinin. The “trunk” contains those conserved parts. The fact that this hemagglutinin “tree” exists in a forest of other hemagglutinins, and neuraminidases (the “N”) with just the crowns showing, and little space between adjacent “trees” gives you an idea of how difficult, or indeed impossible it would be for a B-cell receptor to recognize one of these conserved parts of the protein.
@A R
I thought I had read long ago that the virus wasn’t capable of reassortment, but even now I’m not sure that perhaps I didn’t read that and just guessed. The micrographs of filovirus always seems so smooth & uninterrupted, not like some viruses, so maybe I just assumed it couldn’t be pieced together. It’s good to know for sure, anyway.
Although I knew it was unlikely to develop an airborne, virulent strain, the bit about the reused needles makes me feel much more comfortable. That’s a piece of information I know I didn’t have.
As for the GP stuff goes, I can almost follow. VP30 is just way, way beyond me, but it’s interesting that it interferes with interferon (no, I did not plan that). I wonder how important that is to its destructive cascade?
Anyway, thanks for satisfying my curiosity. Working with pathogens like severe influenzas and filoviruses is something I might have done if my life had gone a bit different my first turn in university. As it is I hardly had any organic chem at all, so most of what I know is just from having a Dr for a dad and random reading of science rags.
The thing is that flu viruses can be carried by birds, and if it doesn’t make them sick, it can be carried by migrating waterfowl. New flus come out of China because pigs, chickens and waterfowl are raised together and because wild fowl passing over can add viruses to the barnyard. They can reassort in the fowl or the pigs (which. are mammals and have a physiology surprisingly similar to that of humans) and come out as something that people can catch. Then if it becomes transmissible, we can have an epidemic. AR and MF Headcase are right, it takes a hardier virus to be survive outside the body long enough to get over an air gap.
Oh for fuck sake, another one?!