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Random Mutation Explanation of Flu Genetics Is Fatally Flawed
Recombinomics Commentary
March 30, 2006
The “random mutation” explanation of pandemic or seasonal flu evolution is almost dead. The recent Canadian swine sequences leave little doubt that almost all rapid genetic change in influenza is driven by recombination.
Earlier comments described recombination in PB2 and PA genes of the swine isolates. However, the recombination is in all eight gene segments and in all seven swine isolates. Isolates from the mid-nineties or earlier with exact matches in the recent swine isolates include A/Fukushima/114/96(H3N2), A/Swine/Tennessee/24/77(H1N1), A/Swine/Tennessee/26/77(H1N1), A/Swine/St-Hyacinthe/106/91(H1N1), A/WI/4754/94(H1N1), A/WI/4755/94(H1N1), A/Swine/Wisconsin/3523/88(H1N1), A/Swine/Iowa/930/01(H1N2).
These data show that recombination is very common and the size of the earlier regions get smaller because of further recombinations within recombinants. The data leaves little room for random mutations.
Similarly, recent isolates of the Qinghai H5N1 bird flu strains show single nucleotide polymorphisms overlaid on the Qinghai background. Virtually all of these polymorphisms are well represented in the sequence database and can be found in other H5N1 on migratory bird pathways.
The data indicate the current explanations of influenza evolution are fatally flawed, yet they are the basis of repeated WHO press releases on the looming pandemic.
A full review of the misconceptions driving vaccine development is long overdue.
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