Check this out if you haven't yet. It took me quite a while since the traffic there must be pretty heavy.
http://www.fluwikie2.com/pmwiki.php?n=Forum.Checkmate
Thanks. I'll try later. I can't even get in right now.
The thing that struck me was that the PB2 E627K modification allows it to retain activity at a lower temperature. If you recall that is what is needed for it to be able to live higher up in our respiratory system. That means that we can sneeze/cough to spread it. Before it was way down in the warmer areas of the lungs and was harder to spread.
From my very limited knowledge of these things, there have been two differences between the H5N1 as expressed in fowl and as expressed in humans.
1) The binding site. Apparently H5N1 lodges in the intestines of fowl, as opposed to the lungs of humans. That is, the binding receptors on the coat of the virus have affinities for different cells in fowl and in humans.
2) The temperature at which the H5N1 likes to live and reproduce--it "likes" the warmer temperatures (say a chicken's gut) and it gets closer to that temperature only in the deep bronchial passages in humans. This means that mere ordinary sneezing and such is less likely to spread the virus outside a human host's body.
So if we have mutations which allow binding *and* breeding in the outermost regions of the human, that would allow greater spread in humans.
The question would then become, is the "cytokine storm" (heightened immune response) deadly in and of itself, or is it most deadly *because* the active sites for the virus are deep in the lungs, and so the immune response leads to drowning in your own fluids...?
Hint: What can the 1918 influenza tell us about this? Has anyone done X-ray crystallography on the proteins of each on e to compare the structures of the two influenza strains?
(...and yes, I *know* with mutation rates as they are, that that is a rather broad brush.)
Cheers!
...oh, and Merry Christmas.