Researchers at the University of Washington report in the April 14, 1997 issue of Virology that they may have an explanation for why the currently approved drug treatment for hepatitis C is ineffective much of the time. The drug, recombinant alpha interferon, is ineffective in 60 to 80 percent of cases.
"This discovery explains the molecular mechanisms for interferon resistance, and points the way to a potential new target for therapeutic drugs to treat hepatitis C," said the principal investigator, Dr. Michael G. Katze (kates), UW professor of microbiology and associate director of the UW's Regional Primate Research Center.
The UW's Office of Technology Transfer has negotiated a patent-based licensing agreement with RiboGene, Inc., a privately-held biotechnology company in Hayward, Calif., which will begin investigating drug therapies based on the UW discovery. Katze is a member of the company's scientific advisory board.
Hepatitis C (formerly called non-A, non-B hepatitis), caused by the virus, affects more than 3.5 million Americans. It is the major reason for liver failure necessitating liver transplants.
"Many viruses that affect humans -- hepatitis, influenza, herpes, HIV, polio and a host of others -- have evolved mechanisms to resist the effects of interferon, one of the body's first lines of defense against viruses," said Dr. Michael Gale, Jr., UW microbiology fellow who is lead scientist and first author of the study. The drug interferon is an artificial version of naturally-occurring interferon, a protein secreted by cells that "interferes with" viral infection and other challenges.
Earlier studies in Japan showed that interferon-resistant HCV strains have a specific RNA sequence within a region of the virus called NS5A. The UW researchers followed up on this research, and tested the ability of NS5A to interact with a key component of interferon response called PKR, a member of an important famil
Contact: Laurie McHale
University of Washington