A recent article published in the open-access journal PLoS
Pathogens maintains that over its evolutionary history,
reassortment of the influenza A virus happens often.
Genetic reassortment is when genetic material mixes from two similar
viruses that are infecting the same cell. Influenza virus A is a
species of virus that causes influenza in birds, humans, pigs, and
horses; it has often given rise to human influenza pandemics.
A team of researchers from both Pennsylvania State University and the
National Institutes of Health (NIH) looked at influenza viruses from
1918 to 2005. They focused on viruses that cause seasonal epidemics in
humans, especially ones that were associated with high mortality.
The severe influenza epidemics of 1947 and 1951, according to the
researchers, were the result of genetic reassortment events. Two human
influenza viruses from the same H1N1 strained switched genetic
material, and thus produced two new hybrid viruses.
It has been unknown as to exactly why very severe influenza epidemics
occur periodically and lead to unusually high illness and mortality
levels - like the ones in 1947 and 1951. The normal model of human
influenza virus evolution argues that major pandemics (of which 1918
was the largest) are due to genetic reassortment of human and avian
(bird) influenza viruses. However, the seasonal influenza epidemics
that occur each winter in the United States are thought to arise
without genetic reassortment.
The new research findings add a layer of complexity to the evolution of
seasonal influenza than was previously believed. That is, within a
single population, multiple
forms of the same strain co-circulate and re-assort. These
quickly-generating, novel viruses are capable of starting major
epidemics.
The authors believe that vaccine design can be helped if intensive
surveillance can capture the full extent of how genetically diverse the
influenza virus is that is co-circulating at a given time.
Multiple Reassortment Events in the Evolutionary History of H1N1 Influenza A Virus Since 1918
Nelson MI, Viboud C, Simonsen L, Bennett RT, Griesemer SB, et al.
PLoS Pathogens 4(2): e1000012. (2008).
doi:10.1371/journal.ppat.1000012
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Written by: Peter M Crosta
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