BETHESDA, Md. A finding by a team of scientists at the National Institutes of Health may account for why the flu virus is more infectious in cold winter temperatures than during the warmer months.
“The study results open new avenues of research for thwarting winter flu outbreaks,” stated National Institute of Child Health Development director Duane Alexander. “Now that we understand how the flu virus protects itself so that it can spread from person to person, we can work on ways to interfere with that protective mechanism.”
Briefly, at winter temperatures, the virus’s outer covering, or envelope, hardens to a rubbery gel that shields the virus as it passes from person to person. With warmer weather, however, the protective gel melts to a liquid phase. But this liquid phase, apparently, isn’t tough enough to protect the virus against the elements, and so the virus loses its ability to spread from person to person.
The findings were published online March 2 in Nature Chemical Biology. The study was a collaboration between researchers at two NIH institutes, the NICHD, and the National Institute of Alcohol Abuse and Alcoholism.
Senior author Joshua Zimmerberg, chief of NICHD’s Laboratory Of Cellular And Molecular Biophysics found that at temperatures slightly above freezing, the virus’s lipid covering solidified into a gel. When temperatures reached about 60 degrees Fahrenheit, the covering began to thaw, and the covering turned to a soupy mix.
Cooler temperatures, apparently, cause the virus to form the rubbery outer covering that can withstand travel from person to person. Once in the respiratory tract, the warm temperature in the body causes the covering to melt to its liquid form, so that the virus can infect the cells of its new host.
“Like an M&M in your mouth, the protective covering melts when it enters the respiratory tract,” Zimmerberg said. “It’s only in this liquid phase that the virus is capable of entering a cell to infect it.
In spring and summer, however, the temperatures are too high to allow the viral membrane to enter its gel state. The individual flu viruses apparently dry out and weaken, and the flu season wanes.
The finding opens up new possibilities for future research, Zimmerberg said. Strategies to disrupt the virus and prevent it from spreading could involve seeking ways to disrupt the virus’s lipid membrane.
In cold temperatures, the hard lipid shell can be resistant to certain detergents, so one strategy could involve testing for more effective detergents and hand-washing protocols to hinder the spread of the virus.
Similarly, Zimmerberg theorizes that in areas affected by a severe form of the flu, people might better protect themselves against getting sick by remaining indoors at warmer temperatures than usual.