Scientists have identified a key factor that determines the ability of influenza viruses to infect cells of the human upper respiratory tracta necessary step for sustaining spread between people. The research, described in the January 6 online edition of Nature Biotechnology and funded by the National Institutes of Health (NIH), offers new insights into how the H5N1 avian flu virus currently circulating in birds would have to change in order to gain a foothold in human populations.
The H5N1 virus has infected several hundred people, but person-to-person transmission has been limited. To trigger a widespread outbreak, experts agree that the bird flu virus must infect the cells lining our noses and throats. We then would spread the virus to others through coughing or sneezing. The latest study, led by Ram Sasisekharan, Ph.D., of the Massachusetts Institute of Technology in Cambridge, refines this notion: The virus can gain access only through a subset of the sugar molecules coating the cells of our upper airways.
"Using an approach that combines experimentation and database analysis, Sasisekharans team has changed our view of flu viruses and how they must adapt to infect us, said Jeremy M. Berg, Ph.D., director of the National Institute of General Medical Sciences, the NIH component that supported the research. The work may improve our ability to monitor the evolution of the H5N1 virus and thwart potential outbreaks.
Chains of sugars called glycans sit on the surface of our cells and control the gates through which different molecules enter. For a virus to gain access to a cell, proteins on the viruss surface must bind to certain glycans.
The binding protein for flu viruses is hemagglutinin. The protein can vary with each flu strain and, as a result, latch on to glycans from different types of cells. While the protein from human-adapted flu viruses favors the sugars dotting the cells of the nose and throat, the one from b
|Contact: Alisa Machalek|
NIH/National Institute of General Medical Sciences