The findings are published in the 2nd March issue of the journal Nature Chemical Biology and are the result of a study carried out by senior investigator and neuroscientist Joshua Zimmerberg and colleagues. Zimmerberg is based at the Laboratory of Cellular and Molecular Biophysics (LCMB) in the National Institute of Child Health and Human Development (NICHD), in Bethesda, Maryland.
Zimmerberg and his team examined the structure of the flu virus, and its outer coat in particular, using nuclear magnetic resonance imaging.
The outer coat of the flu virus, and other respiratory viruses, are made of a fatty protein called hemagglutinin that hardens in cold conditions.
Zimmerberg told Reuters in a telephone interview that this was the "protein we make vaccines against". Hemagglutinin is where the "H" in flu virus names comes from.
When the virus enters a warm host, the hemagglutinin coat melts, and the virus gets to work infecting cells.
Hemagglutinin also helps the virus to bind to the target cell of its host, so the virus can fuse with it and allow its contents to invade the host cell.
During the summer, when the ambient temperature is much higher, the hemagglutinin coat is not able to stay hard and protect the virus, which is more likely to die before it can infect people.
"Like an M&M in your mouth, the protective covering melts when it enters the respiratory tract," Zimmerberg told Reuters.
"It's only in this liquid phase that the virus is capable of entering a cell to infect it," he added.
Duane Alexander, NICHD Director, said these results could suggest new ways to prevent and treat the flu by targeting the hemagglutinin coat.
Scientists have been puzzled for some time about why viruses like the flu are more prevalent in winter, speculating that perhaps it's because people spend more time indoors in confined environments, or because the sun's radiation kills more viruses in the summer. But none of these explanations is entirely satisfactory.
Viruses can't reproduce on their own. They have to enter a living cell and hijack its resources, reprogramming the cell DNA to do its bidding. The new copies of the virus don their hemagglutinin jackets and break out of the cell in large numbers.
The jacket hardens when the virus is shed by the warm host into the cold, so in winter, they stay insulated and alive, increasing the chance of infecting another host.
The jacket does not get hard all at once, Zimmerberg said they observed that it solidifies slowly, from 40 degrees Celsius (104 deg F) down to 4 degrees C (39 deg F). He said he and his colleagues believed this was how the virus managed to stay alive over a range of temperatures.
The researchers suggested that in winter it may even be harder to wash the virus off your hands because in the cold its hard shell protects it against soap and detergents.
"Progressive ordering with decreasing temperature of the phospholipids of influenza virus."
Ivan V Polozov, Ludmila Bezrukov, Klaus Gawrisch & Joshua Zimmerberg.
Nature Chemical Biology, Published online: 02 March 2008.
Sources: Nature Chemical Biology abstract, Reuters.
Written by: Catharine Paddock, PhD