Skip to comments.How Flu Succeeds (Cellular co-option)
Posted on 12/22/2009 7:29:02 AM PST by decimon
Investigators identify host factors that help multiple influenza strains thrive and could be targeted for new antivirals
A JOLLA, Calif., December 21, 2009 -- Investigators at Burnham Institute for Medical Research (Burnham), Mount Sinai School of Medicine (Mount Sinai), the Salk Institute for Biological Studies (Salk) and the Genomics Institute of the Novartis Research Foundation (GNF) have identified 295 human cell factors that influenza A strains must harness to infect a cell, including the currently circulating swine-origin H1N1. The team also identified small molecule compounds that act on several of these factors and inhibit viral replication, pointing to new ways to treat flu. These findings were published online on December 21 in the journal Nature.
Influenza A virus contains only enough genetic information (RNA) to produce 11 proteins and must co-opt host cellular machinery to complete its life cycle. Sumit Chanda, Ph.D., of Burnham, Megan Shaw, Ph.D., of Mount Sinai, John Young, Ph.D., of Salk, Yingyao Zhou, Ph.D., of GNF and others used RNAi screening technology to selectively turn off more than 19,000 human genes to determine which human factors facilitate viral entry, uncoating, nuclear import, viral replication and other necessary functions of the virus.
Because influenza mutates so readily, it has become a moving target for therapeutic intervention, making it difficult to treat circulating strains, including the H1N1 swine flu, said Dr. Chanda. As a result, there is now widespread resistance to two classes of antiviral drugs. However, by targeting more stable human host factors, we may be able to develop therapies that prevent or treat a variety of influenza A strains and are more likely to maintain their effectiveness.
(Excerpt) Read more at burnham.org ...
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