December 13, 2012
Researchers at the University of Southern California (USC) found a trigger that is used by the hepatitis C virus (HCV) to enter liver cells. They discovered that in the early stages of HCV infection, the virus binds to receptors on the surface of liver cells and activates PI3K and AKT, proteins that control cell growth and metabolism, and which allow HCV to enter the cells. According to James Ou, professor of molecular microbiology and immunology at USC's Keck School of Medicine, when the two protein factors are activated, they initiate a group of reactions that alter the physiology of infected cells. Later, by continuing to disturb this pathway, HCV may sensitize the liver cells to become cancerous.
Ou has been studying HCV for 20 years and the hepatitis B virus for 30 years. He explained that the next step is to understand how activation of the PI3K-AKT pathway allows HCV to enter the cell. Ou also noted that the research has led to the identification of a novel target for developing new drugs to treat HCV in the form of compounds that disrupt the PI3K-AKT pathway. These anti-hepatitis drugs would be expected to prevent the virus from entering, and thus, cause the virus to disappear.
The study, "Transient Activation of the PI3K-AKT Pathway by Hepatitis C Virus to Enhance Viral Entry," was published in the Journal of Biological Chemistry (2012;287(50): 4192241930).
No comments have been made.
The content on this page is free of advertiser influence and was produced by our editorial team. See our content and advertising policies.
|How to Reverse Implicit Bias in HIV Care: 6 Steps to Take Today|
|PrEP Prescriptions Rise Sharply, but Unequally, in New York City|
|A Review of Late-Stage HIV Antiretroviral Candidates at IDWeek 2017|
|Free Your (and Carl's) Mind: An Open Letter to Anthony Fauci About HIV Prevention Research Priorities|
|Let's Advance the Conversation Among Black Women on HIV and PrEP|
|This Week in HIV Research: Injectable PrEP Shows Promise in New Study|