Medical expert of the article
New publications
Scientists have explained the mechanism of hepatitis C virus survival in the human liver
Last reviewed: 01.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Viral diseases remain one of the greatest challenges in medical science. Millennia of co-evolution of viruses has contributed to their ability to exploit the human body to survive and reproduce, making treatment difficult.
Scientists from the University of North Carolina (USA) have shown for the first time how small RNA molecules that regulate gene expression in human liver cells are hijacked by the hepatitis C virus to ensure its own survival. The researchers hope that this discovery will help scientists develop new effective antiviral drugs in the near future.
MicroRNAs, involved in the regulation of gene expression in cells, typically block the production of key proteins or destabilize RNAs that encode proteins necessary for cell growth and division. A research team of scientists discovered that binding of microRNA (microRNA-122) in liver cells to viral RNA leads to its stabilization, promoting efficient replication of the viral genome in the liver and supporting the viral life cycle.
"The hepatitis C virus did two very interesting things with microRNA-122," said Stanley M. Lemon, MD, professor of medicine and of microbiology and immunology and a member of the Cancer Center. "First, the virus's interaction with microRNA-122 created a unique relationship with a key regulator, since microRNA-122 makes up about half of all microRNAs present in the liver. Second, the virus hijacked gene expression to its own advantage, disrupting the stability of the RNA and causing the synthesis of viral proteins needed to continue its life cycle. This is a classic example of viruses using useful cellular functions for their own purposes."
Dr. Limon and colleagues' work in 2005 helped demonstrate the importance of microRNA-122 in the self-replication of the hepatitis C virus, but the mechanism by which it did so was not understood. Now, the team has been able to explain this mechanism using a new experimental antiviral drug. The drug, called Antagomere, binds to microRNA-122 and thereby destabilizes the viral genome, accelerating its degradation in the liver.
The results of the latest study are published in the journal Proceedings.
Hepatitis C is a major public health problem that is difficult to detect early on because symptoms do not appear until months or even years after infection. The Centers for Disease Control and Prevention estimates that more than 4 million people in the United States may be infected with the hepatitis C virus, and most of them do not know they are infected. Chronic liver disease and liver cancer may develop in more than a third of cases.
[