Hepatitis C virus attenuates interferon-induced major histocompatibility complex class I expression and decreases CD8+ T cell effector functions
In the present study, researchers investigated the effect of HCV infection on IFN-induced MHC class I expression. They identified the underlying mechanism by which HCV impeded IFN-induced MHC class I expression during infection, and delineated the functional significance of regulation of IFN-induced MHC class I expression. In summary, an immune evasion mechanism of HCV was revealed.
It is quite well known that hepatitis is a major cause of chronic liver disease. Hepatitis C virus (HCV) infects 170 million people worldwide. The majority of HCV-infected patients will progress to chronic hepatitis; 20% of these chronically infected patients develop long-term complications, such as liver cirrhosis and hepatocellular carcinoma. Thus, based on this sizeable medical need, there is a continued need to help understand the underlying biochemistry involved with the nature of the disease and potential remedies.
It is known that major histocompatibility complex (MHC) class I-restricted CD8+ T cells are required for clearance of HCV infection. MHC class I expression is up-regulated by type I and II interferons (IFNs). However, little is known about the effects of HCV infection on IFN-induced expression of MHC class I.
In the present study, we demonstrated that IFN-induced expression of MHC class I is attenuated in HCV-infected cells by activation of PKR, which reduces the effector functions of HCV-specific CD8+ T cells. This appears to be an important mechanism by which HCV circumvents antiviral adaptive immune responses.