Hepatitis C virus (HCV) lingers in the human body for years, slowly
damaging the liver and leading to liver diseases such as hepatitis,
cirrhosis and liver cancer, which is often fatal. Research conducted at
the University of North Carolina at Chapel Hill has discovered a
mechanism that facilitates the virus achieving this life-long
persistence. Chronic HCV infection is the leading cause of liver cancer
in the United States.
“Liver cancer is one of the most important causes
of cancer mortality worldwide. It’s also increasing in rapidly
incidence within the United States, due largely to the spread of HCV
among Americans in the 60s and 70s,” said Stanley M. Lemon, MD,
Professor of Medicine at the UNC School of Medicine and a member of the
UNC Lineberger Comprehensive Cancer Center.
In a paper published online by Nature Medicine this week, a
team led by Dr. Lemon and colleague Daisuke Yamane, DVM, PhD, found that
HCV has a sensor function that allows it to be regulated by the
oxidative damage to cell membranes that occurs as a byproduct of its
replication and the body’s response to it. This slows down virus growth
when oxidative membrane damage becomes too high, but allows it to resume
when the membrane damage is reduced. By auto-regulating its replication
in this way, the virus maintains a low profile, helping it escape
detection by the immune system.