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Swine Flu Chasing the Fickle

July 1st, 2009 by admin | Filed under Swine Flu


Most genetic changes in the flu viruses human, pig, and bird are small and subtle point mutations in the virus’s RNA. Less common but more alarming are sudden, wholesale changes that replace entire genes and are more likely to circumvent the immune system. This process, called genetic shift, is exactly what is now occurring in North American pigs. Thus, the latest swine influenza virus is a curious hybrid: The genes that code for its coat proteins derive from classical swine influenza, but half of its internal genes have been snatched whole from avian and human viruses.

Most commonly, the virus swaps genes that code for its two surface proteins: hemagglutinin (HA) and neuraminidase (NA). Both proteins spike off the virus’s outer coat, and HA initiates infection when it binds to receptors on host cells. The immune system of the infected animal targets sites on these molecules. Therefore, a virus with a novel HA can escape preexisting immune defenses—hence the pig deaths. Influenza viruses are named after their HA and NA components, as in “H1N1” or “H3N2.” Both human and swine influenzas have been historically limited to only a few of these varieties. Birds, on the other hand, can be infected by every combination of the virus’s 15 HA genes and nine NA genes, forming a vast global reservoir of virus. And pigs have receptors for both human and bird flu virus, making them crock pots for new viral combinations.

This season’s variant is an H1N1 with the internal genes of an H3N2. Its HA gene, derived from the classical swine influenza virus, appears to be rapidly mutating. The amount of sequence divergence among certain 2001 isolates “is as much as the difference between classical H1N1 viruses isolated in the 1960s and those isolated in the early 1990s,” Webby reports. If enough point mutations accumulate, that HA molecule could become unrecognizable to the immune systems of both pigs and humans.

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