A genetic flaw in the makeup of the H1N1 flu virus helps explain why the new flu spreads less efficiently than seasonal flu. Scientists for MIT and the CDC say that a surface protein in the virus is not highly proficient at binding to receptors in the human respiratory tract. And that design defect has slowed its transmission around the world.
"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 and the lead MIT author of the study published in Science. A genetic variation in an H1N1 polymerase enzyme has also hampered transmission.
Scientists have been racing to gain a better understanding of the swine flu virus since it first broke out and began to sweep around the globe. At first it appeared relatively lethal, but then researchers determined that the virus was typically mild. Now scientists want to closely watch how it evolves. Viruses often mutate into new forms that make them spread faster. And scientists also want to see if H1N1 becomes more virulent as it adapts.
- check out the report from MIT