December 28th, 2012
Researchers at the University of Southern California (USC) have discovered a trigger by which the hep C virus enters liver cells, giving a clearer picture of how it can begin to damage the liver.
The findings, reported in the 7 December issue of The Journal of Biological Chemistry, may give scientists a target for future development of treatments.
The researchers found that in the early stages of hep C infection the virus sticks to receptors on the liver cells’ surface, activating P13K and AKT, two proteins that control cell growth and metabolism, and that allow HCV to enter liver cells.
“When these two protein factors are activated they trigger a cascade of reactions, altering the physiology of infected cells,” said corresponding author and lead researcher James Ou, professor of molecular microbiology and immunology at the Keck School of Medicine of USC. “Later, by continuing to disturb this pathway, the virus may sensitize the liver cells to eventually become cancerous.”
Ou has been studying hep C for 20 years and hep B for 30 years. This most recent study reflects his long-term interest in understanding the interactions between the two viruses and their host cells, and how they cause liver cancer.
“The next step, which we’ve just begun,” Ou said, “is to understand how the activation of the P13K-AKT pathway allows the [hep c] virus to enter the cell. This research has led to the identification of a novel target for the development of new anti-HCV drugs. Compounds that disrupt the P13K-AKT pathway are expected to prevent the virus from entering liver cells, causing the virus to disappear.”
Research like this is sure to be welcomed by the estimated 150 million people around the world living with the condition. Click here for more information on living with hep C.