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Polymerase Sequences Confirm 1918 Human/Swine Recombination
Recombinomics Commentary
October 5, 2005
It is possible that the high pathogencity of the 1918 virus was related to its emergence as a human-adapted avian influenza virus. These changes may reflect a process of parallel evolution as avian influenza A viruses mutate in response to adaptational pressures, and suggest that the genetic basis of avian influenza virus adaptation to humans can be mapped.
H5N1 is currently acquiring mammalian polymorphisms, which is why several of the mammalian polymorphisms in the 1918 H1N1 pandemic strain are found in H5N1 isolates from Vietnam and Thailand.
However, the 1918 pandemic strain was not an avian strain. It was a recombinant between a swine virus, like the H1N1 classical swine virus from Iowa in 1930, and an H1N1 human virus, like the WSN/33 virus from a human in London in 1933. This observation had been made previously, based on the published sequences of five of the eight 1918 genes.
The same relationship is seen in the three newly published genes, PB2, PB2, and PA. In each case the sequences from H1N1 classical swine and H1N1 human isolates in the early 1930's form complimentary polymorphisms, much like the 2001 H5N1 co-circulating sequences in Hong Kong.
The evolution by recombination is the mechanism of rapid change employed by most if not all viruses. H5N1 efficiently evolves via recombination, and the latest sequences of the three polymerase genes from 1918 show that the same mechanism was used for all eight of the 1918 genes.
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