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I don't think you have a grasp of the data, which is quite straightforward. You are stuck on "random mutations" and "common ancestors" which has NOTHING to do with H274Y in hosts who have not been recently treated with Tamiflu.
it would be much easier to estimate the common anchestor dates,
if we had the full genomes .
Typically we only have HA and NA ~ 22% of the genome
But it seems that everything started in ~mid 2007
in SE-Asia (most new flu strains start in SE-Asia)
And then there was not so much new "creation" of H274Y
mutations. Rather the existing strains did spread
and those with H274Y were more successful.
So, when a new H1N1-strain appears, it might just
overcome the current resistant H1N1 , as that overcame
the old vaccine strains.
Please. The data clearly demonstrates that there is no "common ancestor". H274Y has suddenly appeared in on a variety of genetic backgrounds in isolates from hosts who have not been treated with Tamiflu. These isolates include H5N1 in wild birds in Astrakhan in 2005, clade 2C (Hong Kong) in China in 2005/2006, clade 1 (New Caledonia) in the US in 2006/2007, and clade 2B (Brisbane) in 2007/2008 worldwide. Moreover, within clade 2B there are multiple sub-clades representing independent introductions, as well as recent clade 2C in Hong Kong which includes a reassortant (clade 2C HA with clade 2B NA).
There are too much DATA that refute "common ancestor" and "random mutations". Such posts are now in the nonsense category.
Dominant Tamiflu Resistant H1N1 Sub-clade in Europe Recombinomics Commentary 12:56
October 29, 2008
Recently released NA sequences from H1N1 isolates in Europe in the 2007/2008 season provide more genetic information on the spread of H274Y, which confers Tamiflu (oseltamivir) resistance. Most of these isolates mapped to the same Brisbane/59 sub-clade described previously (see list below).
More recently, isolates in South Africa and Kenya, had a series of changes in this subclade located near the receptor binding domain at position 190 (H3 numbering), raising concerns that the current vaccine, which targets Brisbane/59 may not be as effective this season.
The sub-clade which dominated last season in the northern hemisphere is evolving, and the evolved versions are associated with an increase in H274Y frequency to 100% in South Africa (225/225 sequenced isolates had H274Y).
The dominance of this sub-clade appears to be extending to the current flu season in the northern hemisphere, where the first H1N1 isolates in Canada and the UK have H274Y.
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