The flu's accurate replication process also keeps the virus in check. Given the flu's multiple rounds of RNA replication per infection, too many mutations would result if the process was highly prone to error, leading to catastrophic mutagenesis.
"The perception has always been that the flu virus mutates a lot, and in order to do that it has to have an enzyme that makes a lot of mistakes, but Kim's work shows that is not the case at all," said David Topham, Ph.D., associate professor of Microbiology and Immunology at Rochester and an expert on how the body fights the flu. "There is a selection pressure, perhaps related to the flu's multiple replication strategy, which helps certain mutations develop and avoid immunity so that the virus can spread."
Topham, Kim and John Treanor, M.D., chief of the Infectious Diseases Division of the Department of Medicine at Rochester, lead the New York Influenza Center of Excellence (NYICE), which funded the current research. NYICE is one of five centers nationwide designated by the National Institutes of Health to further our understanding of the flu virus through basic research and surveillance studies, and to facilitate the nation's preparations for a potential pandemic.
To pin down the mechanisms behind flu virus evolution, researchers conducted unique biochemical analyses comparing flu virus replication to HIV replication, which has been well characterized in past research. While both viruses require efficient mutation production to adapt and thrive in their host environments, they replicate their genetic information very differently. HIV has evolved so that the virus only has a few chances to replicate its genome per infection and generate sufficient mutations, while the flu virus has ample chances to make and accumulate genomic mutations in each viral infection cycle.
At the center of the new finding are the polymerases, or enzymes, responsible for viral replication. Because t
|Contact: Emily Butler|
University of Rochester Medical Center