Gnome writes "The 1918 flu caused an unusually high death rate among healthy young adults (ages 15-34). Genomic RNA was recovered several years ago from autopsy material and victims buried in the Alaskan permafrost. The 1918 flu had unique hemagglutinin and neuraminidase proteins on its surface (H1N1). However, they did not cause its pathogenicity because later viruses with this combination are not particularly deadly (e.g., Texas/91). Now, Tumpey and colleagues have reconstructed the entire 1918 virus and tested it. Unlike current flu viruses, the 1918 virus does not require an exogenous protease to infect cells in culture. Moreover, all 13 mice infected through the nose by the 1918 virus developed severe lung inflammation and died within 7 days, while none infected with the Texas/91 strain died. Surprisingly, recombinants between 1918 flu and Texas/91 suggest that the viral polymerase acts in concert with the other 7 proteins to increase virulence. On the bright side, existing antiviral drugs and a novel siRNA therapy were previously shown to protect mice against certain 1918 recombinant viruses.
Tumpey et al., "Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus" Science. 2005 Oct 7;310(5745):77-80.
Sunday, January 21, 2007
Biology of the 1918 Flu
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polymerase - faithful copy
In this Nature paper by Taubenberger et al., they analyzed the sequence of the entire 1918 viral genome. They found that the 3 polymerase subunits of 1918 flu have only 10 amino acid changes from an avian flu. They conclude that this is "consistent with the hypothesis that they were derived from an avian source shortly before the pandemic."
They also note that "a number of the same changes have been found in recently circulating, highly pathogenic H5N1 viruses".
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