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Novel H1N1 virus linked to 1918 pandemic

7/13/2009

WASHINGTON Several research groups funded by the National Institute of Health’s National Institute of Allergy and Infectious Diseases and National Institute of General Medical Sciences recently have put together a picture of where the novel H1N1 virus came from and how it evolved, the agency noted in a report published on its Web site Monday.

They discovered that the novel H1N1 virus is a descendent not only of swine viruses but also of the H1N1 virus that caused the 1918 pandemic, which killed more than 40 million people worldwide.

“The 1918-1919 influenza pandemic was a defining event in the history of public health,” stated NIAID director Anthony Fauci. “The legacy of that pandemic lives on in many ways, including the fact that the descendents of the 1918 virus have continued to circulate for 9 decades.”

In other work, 2 research groups — an NIGMS-funded team at the Massachusetts Institute of Technology and researchers at the Centers for Disease Control and Prevention — recently collaborated to test the ability of novel H1N1 to spread and cause disease. They isolated viruses from 3 patients and infected mice and ferrets. The results were published in the July 2 issue of Science.

The researchers found that compared with seasonal H1N1 flu viruses, the novel H1N1 viruses replicated to higher levels in lung tissue and were also more deadly. The scientists also found the viruses in the intestinal tracts of the ferrets, which might explain reports of gastro-intestinal problems in some infected people. However, the novel H1N1 viruses transmitted less efficiently between ferrets in respiratory droplets than seasonal H1N1.

The binding of influenza viruses to their target cells is mediated by hemagglutinin. The researchers found that the novel H1N1 hemagglutinin binds to receptors in the human respiratory tract much less effectively than other flu viruses that infect humans. However, flu viruses can mutate rapidly, so the virus could potentially improve its ability to bind, researchers cautioned.

The researchers also found that novel H1N1 doesn’t have a version of another gene called PB2 that has been associated with efficient virus transmission. However, they point out that the virus could acquire another version of the gene through mutation or by exchanging genes with other influenza viruses.

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