A team from MIT and the Centers for Disease Control and Prevention has found a genetic explanation for why the H1N1 "swine flu" virus spreads from person to person less effectively than other flu viruses.
The virus has a form of surface protein that binds inefficiently to receptors found in the human respiratory tract, the team reports.
"While the virus is able to bind human receptors, it clearly appears to be restricted," says Ram Sasisekharan, the Edward Hood Taplin Professor and director of the Harvard-MIT Division of Health Sciences and Technology (HST) and the lead MIT author of the paper.
According to Sasisekharan, the weak binding, along with an H1N1 polymerase enzyme, explains why the virus hasn't spread as efficiently as seasonal flu.
However, flu viruses are known to mutate rapidly, which increases the concern for the H1N1 virus mutating to improve its binding affinity. Sasisekharan says, "We need to pay careful attention to the evolution of this virus."
Researchers also discovered the N1N1 strain has substantial genetic variability in the proteins targeted by current vaccines - making it likely the existing vaccines will be ineffective against the new strain, should the virus mutate. They fear the new strain might just need a single change or mutation that could cause the vaccines to be ineffective.
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