A team from MIT and the Centers for Disease Control and Prevention has found a genetic explanation for why the new H1N1 "swine flu" virus has spread from person to person less effectively than other flu viruses.
The H1N1 strain, which circled the globe this spring, has a form of surface protein that binds inefficiently to receptors found in the human respiratory tract, the team reports in the July 2 online edition of Science.
That restricted, or weak, binding, along with a genetic variation in an H1N1 polymerase enzyme, which MIT researchers first reported three weeks ago in Nature Biotechnology, explains why the virus has not spread as efficiently as seasonal flu, says Sasisekharan. However, flu viruses are known to mutate rapidly, so there is cause for concern if H1N1 undergoes mutations that improve its binding affinity.
The H1N1 strain, which circled the globe this spring, has a form of surface protein that binds inefficiently to receptors found in the human respiratory tract, the team reports in the July 2 online edition of Science.
That restricted, or weak, binding, along with a genetic variation in an H1N1 polymerase enzyme, which MIT researchers first reported three weeks ago in Nature Biotechnology, explains why the virus has not spread as efficiently as seasonal flu, says Sasisekharan. However, flu viruses are known to mutate rapidly, so there is cause for concern if H1N1 undergoes mutations that improve its binding affinity.
