A genetic explanation for why the new H1N1 "swine flu" virus has spread from person to person less effectively than other flu viruses has been espoused by US scientists.

A collaborative team of researchers from the Massachusetts Institute of Technology (MIT) and the Centers for Disease Control and Prevention have found that 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.

"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.

He points out that that restricted binding, along with a genetic variation in an H1N1 polymerase enzyme, which was first reported about three weeks ago in Nature Biotechnology, explains why the virus has not spread as efficiently as seasonal flu.

However, flu viruses are known to mutate rapidly, so there is cause for concern if H1N1 undergoes mutations that improve its binding affinity.

"We need to pay careful attention to the evolution of this virus," says Sasisekharan.

For their study, the researchers compared the new H1N1 strain to several seasonal flu strains, including some milder H1N1 strains, and to the virus that caused the 1918 flu pandemic.