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Infection with the hepatitis C virus (HCV) causes acute hepatitis. This disease has a high probability of becoming chronic and leading to cirrhosis, but a more deadly consequence is hepatocellular carcinoma. Interferon α (IFNα)-based treatment combined with ribavirin is the major therapeutic choice available for the treatment of chronic HCV infection.

The scavenger receptor class B type I (SR-BI) or its human homologue CD36 and LIMPII Analogous-1 (hSR-BI/CLA-1) has recently been shown to interact with HCV envelope glycoprotein E2, thus suggesting that it might participate in entry of the virus into host cells. This rationale underlies current interest in the potential role of IFNα in hSR-BI/CLA-1 expression in HepG2 cells.

It was shown that endogenous hepatocyte expression of hSR-BI/CLA-1 was suppressed by exposure to IFNα …