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Since December, an outbreak of swine flu in India has killed more than 1,200 people, and a new MIT study suggests that the strain has acquired mutations that make it more dangerous than previously circulating strains of H1N1 influenza.The findings, which appear in the March 11 issue of Cell Host & Microbe, contradict previous reports from Indian health officials that the strain has not changed from the version of H1N1 that emerged in 2009 and has been circulating around the world ever since. With very little scientific data available about the new strain, the MIT researchers stress the need for better surveillance to track the outbreak and to help scientists to determine how to respond to this influenza variant.
“We are re really caught between a rock and a hard place, with little information and a lot of misinformation,” says Ram Sasisekharan, the Alfred H. Caspary Professor of Biological Engineering at MIT and the papers senior author. “When you do real-time surveillance, get organized, and deposit these sequences, then you can come up with a better strategy to respond to the virus.”
In the past two years, genetic sequence information of the flu-virus protein hemagglutinin from only two influenza strains from India has been deposited into publicly available influenza databases, making it difficult to determine exactly which strain is causing the new outbreak, and how it differs from previous strains. However, those two strains yielded enough information to warrant concern, says Sasisekharan, who is also a member of MIT & Koch Institute for Integrative Cancer Research. He and Kannan Tharakaraman, a research scientist in MIT & Department of Biological Engineering, compared the genetic sequences of those two strains to the strain of H1N1 that emerged in 2009 and killed more than 18,000 people worldwide between 2009 and 2012.The researchers found that the recent Indian strains carry new mutations in the hemagglutinin protein that are known to make the virus more virulent. Hemagglutinin binds to glycan receptors found on the surface of respiratory cells, and the strength of that binding determines how effectively the virus can infect those cells.
One of the new mutations is in an amino acid position called D225, which has been linked with increased disease severity. Another mutation, in the T200A position, allows hemagglutinin to bind more strongly to glycan receptors, making the virus more infectious.