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Friday, April 18, 2003The immune system has many ways to detect and fight off invading microbes, and microbes have just as many ways to elude and disarm immune system components. Through a series of experiments on cells grown in the laboratory, Drs. Gale and Lemon defined the strategy HCV uses to evade the host's immune response. As HCV begins to replicate in its human host, it manufactures enzymes, called proteases, which it requires to transform viral proteins into their functional forms. The Texas investigators determined that one viral protease, NS3/4A, specifically inhibits a key immune system molecule, interferon regulatory factor-3 (IRF-3). IRF-3 orchestrates a range of antiviral responses. Without this master switch, antiviral responses never begin, and HCV can gain a foothold and persist in its host. Next, the scientists searched for ways to reverse the IRF-3 blockade. They applied a protease inhibitor to human cells containing modified HCV. This prevented the virus from making functional NS3/4A and restored the cells' IRF-3 pathway. Follow-up studies have shown that once restored, the immune response reduced viral levels to nearly undetectable levels within days, according to Dr. Gale. The identification of this viral protease-regulated control of IRF-3 opens new avenues in both clinical and basic research on hepatitis C, notes Dr. Gale. Until now, scientists had not considered the possibility that inhibiting this protease did anything more than halt viral replication. "Now that we know NS3/4A inhibition essentially restores the host's immune response to the virus, we can assess hepatitis drug candidates for this ability as well," Dr. Gale says. This is fantastic news. It will lead to a whole new way of thinking about treatment and drug development. Stay tuned.... posted by Sydney on 4/18/2003 08:37:00 AM 0 comments 0 Comments: |
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