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Hepatitis C's interferon resistance mechanism discovered

July 2, 1999--Though interferon, the body's naturally occurring antiviral agent, is the mainstay treatment for hepatitis C virus (HCV), it cures only 20 percent of infected patients. The reason, according to new research, may be that HCV can mimic one of the molecular targets of interferon and may block its ability to kill viruses.

"Not only have we solved a major clinical problem relating to the treatment of HCV, but researchers may be able to use this information to develop more effective HCV therapies," said Michael Lai, the leader of the scientific team that made the discovery and an HHMI investigator at the University of Southern California School of Medicine.

Nearly four million people in the United States alone suffer from HCV infection, which results in 10,000 deaths a year from cirrhosis, liver failure or liver cancer. The virus is spread through intimate sexual contact, needle sharing, and blood products.

Chronic HCV infection, which develops in 80 percent of patients, progresses slowly. Indeed, patients can remain symptom-free for 20 years or more following infection, but the virus eventually attacks the liver. A large percentage of patients who are currently waiting for liver transplants are infected with HCV. In the United States, treatment of chronic HCV infection costs an estimated $600 million annually.

During the initial stages of HCV infection, interferon -- produced by certain fibroblast and immune system cells -- does its job by binding to receptors on the surface of HCV-infected liver cells. This triggers the infected cell to produce protein kinase (PKR), an enzyme that adds a chemical entity known as a phosphate group (a process called phosphorylation) to a variety of proteins, including itself.

Among PKR's targets is a protein called eukaryotic initiation factor 2 (eIF2a ). Adding a phosphate group to eIF2a turns off protein synthesis within
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
2-Jul-1999


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