Posted on 05/09/2005 10:18:08 AM PDT by Dog Gone
Some folks suggested that we begin a thread similar to the Marsburg Surveillance Project for monitoring developments regarding Avian Flu.
The purpose is to have an extended thread where those interested can post articles and comments as this story unfolds.
If we're lucky, the story and this thread will fade away.
Man, I hate to read this.
All? No.
At least not right now.
Actually this is the part that bothered me more. Some drugs we have been talking about are now being recognized as not working, much like we suspected.
No.
The Lucky Ones will live. By making some preparations and educating yourself as to what is necessary for survival, you can improve your odds.
Yes, eventually, one way or another.
Damn.
the bloc's members have been jolted into a more active response to the danger
Why is apathy such a part of human nature? Or, perhaps, it's a innate part of government. Either way, why does it take a jolt to to see a response is needed?
Sorry, all rhetorical. Early morning, pre-coffee, mini-rant.
I read a article a few days ago about North Carolina chicken processors. No one in the factory knew about the pending dangers of their profession and H5N1. No one in management had put any testing measures in, etc.,etc.
Yes.
With great respect, "Unseen's" critique is MOSTLY incorrect from the scientific perspective (I am trying to avoid politics as I always try to do in my FR postings).
First he writes:
"while sick birds can not fly those that have been infected and survive can still shed the virus. Also many birds coexist with the virus in their gut and thus are not killed off. They are the natural reservoir for Flu. Among these are waterfowl. Also from my understand it is the H not the N that cause immunity."
Comment: There is no evidence that antibodies against "H" (hemaglutinin) are more important than antibodies against "N" (neuraminidase) -- both, by the way are unfortunate names because they imply a functionality (observed originally in test tubes in the 1950s that have nothing to do with the actual functionality of these two key viral proteins). While it is certainly taught in medical school that "H" protection is the more important, a review of the literature shows no support for this. Rather, anti-"N" antibodies are JUST as protective as anti-"H" at least in experimental studies in animals (which are impossible to do in humans).
The best references in support of this point are:
Chen Ze. "Influenza DNA vaccine". Chinese Medical Journal 2004; 117(1): 125-132.
and
Johansson BE et. al. "Supplementation of conventional influenza A vaccine with purified viral neuraminidase results in a balanced and broadened immune response." Vaccine 1998; 16: 1009-1015.
[I hope there will be no disparaging of the first piece because it comes from China. They do some of the best work available on influenza and this specific article reviews the "western" literature on the subject as well].
However, I DO agree with Unseen that geese, ducks, and probably other long distance migratory fowl still carry H5N1, BUT it is obviously changed to become less lethal. Whether or not it is STILL lethal to chickens remains unknown in its new mutation (though my guess is that it is). But to humans? No reason to believe that which bring me to Unseen's second point. He writes:
"however, the recent scientific study of the 1918 flu shows that no re assortment is necessary. And thus the Bird flu of 2005 resembles that of 1918 very closely. This is not the same as flipping a coin in that regard. We have a pandemic of FLU every year. Tens of thousands die. The difference between the yearly pandemics and the 1918,1957 and 1968 pandemic is that a Flu virus mutated significantly enough so that our bodies could not readily identify the virus. Thus more people died of the Flu in those years. With 1918 being totally different and killing upwards of 50 million. The difference wit turns out was a complete jump from bird to human. Much like what is occurring in 2005."
Comment: As Jeffrey Tautenberg who sequenced the 1918 flu virus remarked (I'm paraphrasing): "there are H5 amino acid (receptor) sequences that are seen in the 1918 flu. However there are MANY oddities in the 1918 flu structure that are NOT replicated in any of the multiplicity of H5N1 strains yet isolated. So while it is likely that at least SOME of the 1918 mutations seen in the H5N1 strains of today MAY explain the very rare transmission from birds to humans, what we do not know is how many more mutations in H5N1 will be necessary to make transmissiion truly efficient from birds to human (it distinctly is NOT efficient -- see below) or from human-to-human (which is VERY VERY inefficent).
Thus, from the very guy who painstaking sequenced the entire 1918 geneome it is incorrect to state that it "resembles the H5N1 virus quite closely". This is wrong from both the absolute (that is, genomic) sense and, more important from the much-more-complicated "functional" sense which is clearly not a linear sum of gene changes.
Unseen also writes in critique:
"The conditions not only exist today but are far worse in many parts of the world. China, India, Indonesia, major African cities, Mexico, Brazil, New York, London and on and on. All of these Cities and Countries have huge populations packed together in close quarters. In 1918 the rural population was 80% and 20% in cities today that is switched."
Sorry, that's just wrong. Here's why: while it is true that there are crowded cities in China, India, etc., simple arithmetic shows that the density of population is orders of magnitude below the three primary "hot spots" for 1918 flu: troop ships, trenches, and worst-of-all, hospitals (run the numbers for people per square mile in the huge hospital wards/tents of 1918 and you'll find it is tens of millions per square mile, MUCH higher than any of the places that Unseen has named). Further, mobility -- that is, dynamic separation -- among individuals was IMPOSSIBLE in any of the 1918 settings mentioned above, whereas even in Dehli and Peking, mobility is the rule resulting in a time-averaged overall separation that is much much greater than what obtained in 1918.
Finally, 1918 tenaments in most inner cities had (a) almost non-existent sanitation; (b) no air handling of any kind except for opening or closing windows; (c) an absence of surface disinfectant use.
Now I'm not here to say that there are not SOME places in SE Asia that are every bit as bad as the inner city living conditions in the US in 1918. What I AM saying, however, is that even IF H5N1 breaks out in SE Asia and IS brought by plane to the US, individuals will be quickly isolated and treated (if only in their own homes). If a lethal clone of the virus kills the host, end of game for the virus. Instead, we'll see what we saw in Peru in 1994 (hardly a bastion of cleanliness) with cholera: initially awful until people moved to Chile where the water treatment (in this case, the vector for disease rather than the air) was much better. Within a few weeks, the cholera organism had reverted to a benign form (that is the deadly clones died out). Why? Because unless there was a relatively HEALTHY host who was mobile (i.e. not dying from pneumonia) the organism had no way to spread. So, lethal clones evaporated and mild-disease clones replaced it.
Bottom line: it is (a) VERY high density crowding and (b) lack of mobility that promote lethal strains of any organism, simply because another susceptible host is inches away requiring no movement on the part of the original host. Thus, the clone (and there are many in any infection, especially with highly mutable organisms such as influenza) that wins out is the one that multiplies most quickly which, by definition is most damaging to the host (since the organism is obligately intracellular and thus kills many, many more host cells resulting in disease symptoms and finally death). Conversely, with even modest separation of people (the "range" of the virus as an aerosol is probably measured in meters or less in most cases and is very susceptible to UV and moisture as would occur outdoors) OR with modest air filtration (as occurs on airplanes and in most -- though not all -- residential buildings even in China), the organism is forced to a less lethal state by natural selection of clones that don't cause immobility (severe disease) in the host.
Bottom line: if you are an immobilized chicken in a chicken house with 10,000 - 100,000 other chickens, you are probably in trouble. If you are a human, you are not.
The best data we have on human-to-human transmission comes from Thailand (reference: "Seroprevalence of anti-H5 antibody among Thai Health Care workers after exposure to Avian Influenza (H5N1) in a Tertiary Care Center" Clinical Infectious Diseases 2005;vol 40. page e16-
e18). In this -- the ONLY seroprevalence study looking to see if humans exposed to patients with virulent H5N1 even got infected, let alone got sick -- the answer was that out of 50 professional staff an non-professional staff in a referral hospital caring for H5N1 victims, there was ZERO (0%) seroconversion. Now the numbers (50) are not large, but a simple statistical confidence calculation shows that at worst the highest percentage transmission rate consistent with this data is 3%. Hardly the stuff of pandemics. Could it change? Sure. Has it changed in SIX years? No.
One final point: there have been TRILLIONS (yes, TRILLIONS) of interactions between humans and live chickens in animal markets and farms in SE Asia in the past 6 years since H5N1 was discovered (this time frame is very long -- eons by viral evolutionary standards) yet there have been only about 100 cases of bird-to-human transmission. What would explain this?
1. Partial to near complete immunity to N1 because of the presence of H1N1 in the environment (and in all vaccine preparations) for more than 2 decades. This may explain why younger people tend to get sick (because they either haven't been vaccinated or been around long enough to get natural exposure to human-to-human transmission of garden variety H1N1
2. Extremely ineffective binding of current H5 protein types (or strains, if you like) to human respiratory cell receptors.
3. Cross reactivity of OTHER "H" antibodies in humans to H5.
In order to resolve the debate over whether or not the sky is falling with H5N1, we must do two things:
(a) get data on seroprevalence across a small statistical sample (say 1 - 2%) of large populations stratified by contact with chickens or not and also stratified by age
(b) establish robust, real-time surveillance of BOTH human and animal SYMPTOMS consistent with bad flu. That is why my scientific work -- outlined in the book "Microbe: Are we ready for the next plague?" is focused on implementing electronic disease reporting, ESPECIALLY in areas in the US where migratory bird paths exist: the pacific coast, the central US flyway and the eastern flyway, and including surveillance of multiple animal species (birds and mammals) and humans.
We have been successful in the latter in California and west Texas (http://syris.arescorporation.com/demo). We hope to expand the system -- which is very cost effective and which was used with great effect in managing medical problems of Katrina evacuees as well (see Albuquerque Journal Business Outlook of Oct 10, 2005) -- shortly. (The Albuquerque Journal reference is: http://www.abqjournal.com/biz/outlook/397454outlook10-10-05.htm. I think it requires a subscription, but I think I can post the article if I get permission from the Journal or maybe Free Republic has a policy on posting the entire text of articles, but I don't know what it is).
So, let's keep the debate open and as scientific as possible. I disagree with Unseen on all points except that it IS true that migratory birds ARE carrying H5N1 -- but clearly NOT the same H5N1 as was KILLING those same migratory birds just a few months ago. What difference this will ultimately make can only be determined with the two data-gathering approaches I have outlined above.
I have not been following this thread as I should, but it is so long, there is no way I can read it all. Is there a way to find the posts that relate to alternative medicines (like elderberry) and preparations for quarrantine without reading the whole thing? Sorry, I just don't have time to start at the beginning.
I'm not sure how you are using the word "clone" in your post. Would you explain? Thank you for participating, all information is welcome.
-bc
Well, if "scientific" is the criterion, then we need to be careful and clear in what words we use. "Clone" is something entirely different than "strain."
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We are sooooo screwed
So do any Canadian Geese have it yet...that would truly suck on a grand scale...
I thought the 1918 flu had somewhere in the range of 12-15% fatality.
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