Researchers identify potential new target for treating h... ( SALT LAKE CITY A team of scientists...)

Researchers identify potential new target for treating hepatitis C

Date:3/29/2010

SALT LAKE CITY A team of scientists including University of Utah researchers has discovered that binding of a potent inhibitor of the hepatitis C virus (HCV) to the genetic material of the virus causes a major conformational change that may adversely affect the ability of the virus to replicate. This discovery, published in the March 29 early edition of the Proceedings of the National Academy of Sciences, provides a potential new target for structure-based design of new hepatitis C treatments.

Hepatitis C is a major public health problem affecting as many as 170 million people worldwide, with 2 million to 3 million new cases diagnosed each year. In the United States, HCV infection is the major cause of liver cancer and liver transplantation and it results in the death of approximately 10,000 people each year. Currently, the most effective treatment for hepatitis C is an agent called pegylated interferon, which is often combined with an antiviral drug called ribavirin.

"The available therapies for hepatitis C infection have limited effectiveness, with less than a 50 percent response," says Darrell R. Davis, Ph.D., the lead author and professor and interim chair of medicinal chemistry and professor of biochemistry at the University of Utah. "However, small molecules that inhibit viral replication have been reported and they represent potential opportunities for new, more effective HCV treatments."

HCV is a member of the Flaviviridae family of viruses, which also includes the viruses that cause yellow fever and dengue. There are six major genotypes of HCV, which differ slightly in their genetic constitution and vary in their response to treatment. HCV has a single strand of ribonucleic acid (RNA) as its genetic material and the virus replicates by copying this RNA. Previous research has shown that the three-dimensional structure of HCV RNA appears to be crucial for initiating the viral replication process.

Davis and his
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Contact: Phil Sahm
phil.sahm@hsc.utah.ed
801-581-2517
University of Utah Health Sciences
Source:Eurekalert

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