Avian Flu Pandemic?

[Skeptic Ginger]

....

But in its current form, the virus doesn't easily bind to the receptors found in the human upper respiratory tract, so how it has managed to infect humans remains an open question. Of all the people who have frequent contact with birds, only a vanishingly small number have become infected with H5N1. Did they become infected because they recieved an unusually high exposure? Because of a genetic predisposition -- say, a different ratio of ciliated versus non-ciliated cells? Because of some rare behavior that enabled the virus to reach the deep lung, where the cells with the receptors it likes are found? Because the virus they were exposed to represented a mutant strain with better affinities for human receptors? We just don't know.

While some of the details of some of the exposures are unknown, your statement, "we know darn little" is what I take issue with. Given the case which was found to have an encephalitis presentation instead of pneumonia, and the cases where drinking contaminated raw duck blood seemed to be the only exposure, I think infection via the GI tract is highest on the differential. (Cooked poultry is not an issue). The genetic susceptibility is suggested by seeing more blood relatives infected in groups than non-blood relatives. Sample size is too small for conclusions. Inhaling particulates that reach deep in the lung such as with mycobacterium TB give a clear model how such infections are transmitted. The fact chicken droppings result in lots of fine particulates as well as recovery of the virus from the droppings suggests inhalation of concentrated amounts as the cause for the pattern of epidemiology seen. Haanta virus has similar epidemiology.

You can argue none of this is proved or even confirmed. But to say we know darn little implies a lot more mystery than I think is warranted.

 

[Skeptic Ginger]

Recombination, reassortment and mutation are all different. The virus exists as eight separate RNA strands. Reassortment usually means a mix and match of eight unsegmented strands. Recombination is snips of the strands being traded between strands. (There are better descriptions elsewhere.) Niman pushes the recombination theory of influenza evolution.

Many individual cases (your Nigeria example) may not mean anything more than many individual b2h. A large cluster is more likely to point to h2h2h2h.

You know the Nigeria case example was hypothetical, I hope. There are no recorded human cases in Nigeria though as I said, some of us think that means underreporting not lack of cases.

Reassortment and mutation have been clearly documented. And I know about gene transfer in other organisms and viruses. Are there flu strains with known recombination patterns? I've not yet heard this hypothesis mentioned with influenza studies.

 

[Dymanic]

You can argue none of this is proved or even confirmed. But to say we know darn little implies a lot more mystery than I think is warranted.

Let's not quibble over semantics. My "we know darn little" was just a rhetorical device I often use, a rephrasing of the post I was responding to. I concede that the result here came off a little too strong. "There are numerous uncertainties" is all I meant to imply. Just as is the case with an approaching hurricane, proof and confirmation may turn out to be fatally expensive luxuries when it comes to dealing with this virus.

There are essentially two approaches here. One is to assume that H5N1 will act like other influenza viruses, at least once (if) it emerges in a pandemic form. The other is to assume that it will continue to do what it has been doing up till now, which is to confound the experts at every turn. Each approach involves a certain margin of error, and thus incurs certain risks.

Sample size is too small for conclusions.

Small sample size hasn't been much of an obstacle to the forming of conclusions, if the plethora of ravings all over the media and the net are any indication. Whether those conclusions are strongly supported by evidence is another matter entirely.

The genetic susceptibility is suggested by seeing more blood relatives infected in groups than non-blood relatives.

I personally favor the genetic susceptibility hypothesis. Another interpretation, of course, is that such clusters represent exposure to a common source -- and yet another is that they represent H2H transmission.

Are there flu strains with known recombination patterns? I've not yet heard this hypothesis mentioned with influenza studies.

Recombination is a well accepted means of transfer between strains of influenza virus. What is in dispute is whether it is significant as a means of transfer. Henry Niman claims to have conducted analysis of the patterns sufficient to produce an understanding of "The Rules" by which recombination occurs, but as he is using his findings as the basis for a commercial enterprise, he isn't giving up what "The Rules" are. Most of the leading virologists remain skeptical -- or at least agnostic -- with regard to Niman's theory, but he cannot easily be dismissed as a crackpot; he has the credentials.