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Study details hepatitis C ability to block immune system response

The study was published in an advance online edition of the Proceedings of the National Academy of Sciences on May 17.

Hepatitis C virus (HCV) is a worldwide public health problem. The World Health Organization estimates that 170 million people worldwide are chronically infected and that between 3-4 million are newly infected annually. HCV is the leading cause of chronic liver disease including hepatic fibrosis, end-stage cirrhosis, and hepatocellular carcinoma. There is no vaccine available to prevent HCV, and current therapies are costly, have serious side effects and are curative in only a fraction of patients. According to the World Health Organization, the major causes of HCV infection are use of unscreened blood transfusions, and re-use of needles and syringes that have not been adequately sterilized.

Viral infections like hepatitis C often trigger an immediate innate immune response involving release of type 1 interferon (IFN-? and IFN-?). In turn, type 1 interferon stimulates the production of a family of what are known as IFN stimulated genes that have a multitude of inhibitory effects on viral replication in infected and neighboring uninfected cells. While interferon production and other immune responses can greatly influence the course of a number of different viral infections, many human pathogenic viruses have evolved distinct strategies to inhibit the early signaling events leading to interferon production. HCV is no different.

"We have previously demonstrated that many interferon stimulated genes with antiviral activity are induced in the liver during HCV infection," said Francis V. Chisari, M.D., a Scripps Research professor whose laboratory conducted the study. "Despite their induction, the virus can persist indefinitely, indicating that it is resistant to their antiviral effects."

The current study sheds light on one strategy the hepatitis C virus uses to resist the immune system. The findings suggest that the hepa
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
18-May-2006


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