Hepatitis C Virus, Inflammation, and Cellular Aging: Turning Back Time

Abstract

There is evidence that hepatitis C virus (HCV) infection, like HIV infection, may be associated with chronic inflammation, immune activation, and immune senescence, which contribute to increased risks for cardiometabolic or other diseases outside the liver, as well as to ongoing damage in the liver. These effects may persist after a sustained virologic response (SVR) is achieved with HCV therapy. Such findings support initiation of treatment for HCV-infected individuals before damage to the liver is apparent and monitoring of individuals for complications even after an SVR is achieved. Fibrosis is not always reversible after SVR is achieved, and this should serve as an argument against waiting until fibrosis develops before initiating treatment for HCV-infected individuals. This article summarizes a presentation by Susanna Naggie, MD, MHS, at the IAS-USA continuing education program, Management of Hepatitis C Virus in the New Era: Small Molecules Bring Big Changes, in New York, New York, in September 2015.

Figure.

The relationship between inflammation, immune activation, and immune senescence. CMV indicates cytomegalovirus. Adapted from Hearps et al.