My understanding of the mutation is something along these lines
http://www.fluwikie.com/index.php?n=Science.InfluenzaPrimerII
There are sialic acids found on the surfaces of alpha 2,3 galactose and alpha 2,6 galactose receptors that the H5 protein in H5N1 binds to. Bird flu can dock/bind to alpha 2,3 galactose receptors right now, but not alpha 2,6 galactose . The fear is that a virus will mutate and be able to dock at alpha 2,6 galactose receptors, and then it will be transmissible from human to human. Both pigs and humans have both alpha 2,3 and alpha 2,6 receptors, so if a pig or a human suffers from both avian flu and the regular flu at the same time, there could be genetic mixing and an avian flu that can attach to the alpha 2,6 receptor will be created.
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Don’t we have alpha 2,6 sialic acid receptor blockers that we could use to prevent the spread of the flu? Block the receptor and the flu can’t get in.
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Whats a battle?
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Why can’t we create antibodies for the H5 protein if it is always going to go in through the same receptor, the sialic acid on the surface of an alpha 2,6 receptor?
I don’t know tons about cellular biology so some of my info may be wrong.