A Stanford University researcher’s recent discovery of a genetic link to the progression of the hepatitis C virus (HCV) may have positive therapeutic implications. Peter Sarnow, PhD, professor of microbiology and immunology at Stanford University School of Medicine in California, explained that by inactivating a component of RNA (ribonucleic acid) found in the liver known as miR-122 (microRNA), his laboratory was able to reduce overall HCV RNA presence by 80%. The ability to significantly reduce this material is a potential breakthrough, considering that HCV is an RNA-linked virus that relies on the genetic information found in miR-122 to grow and replicate.
“If you can lower the amount of the microRNA in the liver without affecting liver function maybe this will help lower the viral load,” said Dr. Sarnow, who reported his initial findings in the September 2005 issue of Science. The report represented the first-ever link made between the presence of microRNA and a major infectious disease.
Dr. Sarnow presented his latest findings at the Experimental Biology Meeting in San Francisco on April 5, 2006. In addition, Stanford University has reached a licensing agreement with Alnylam Pharmaceuticals and Isis Pharmaceuticals. Both companies are interested in developing a new HCV therapy based on the manipulation of microRNA levels in the liver to block progression of the virus. Potential complications related to a microRNA-based treatment, such as cancer, have not yet occurred in animal experiments conducted by Alnylam and Isis.
Chronic HCV often leads to life-threatening complications such as cirrhosis (liver scarring due to fibrosis and nodules), liver cancer, and ultimately a degeneration of all liver functions. HCV is the most common blood-borne virus in the U.S., killing more than 10,000 people per year.
Source: Medical News Today, April 10, 2006