Hepatitis C viral proteins interact with Smad3 and differentially regulate TGF-beta/Smad3-mediated transcriptional activation.

Transforming growth factor-beta (TGF-beta) is a pleiotropic cytokine implicated as a pathogenic mediator in various liver diseases. Enhanced TGF-beta production and lack of TGF-beta responses are often observed during hepatitis C virus (HCV) infection. In this study, we demonstrate that TGF-beta-mediated transactivation is decreased in cells exogenously expressing the intact HCV polyprotein.