- "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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