It is known that the production of and/or response to interferon (IFN) are deregulated during
chronic hepatitis C virus (HCV) infection. In particular, several studies have shown that patients
with chronic HCV infection who have a high natural level of IFN-stimulated genes (ISGs) do not
achieve viral clearance and have a poor response to treatment with pegylated IFNα and ribavirin. The
viral and/or host factors that are responsible for the higher endogenous ISGs expression in some HCV
infected patients compared to others remain to be determined. However, type III IFNs, and in particular
the new discovered IFN lambda (L) 4 Gene, appear to play a dominant role in driving ISGs response
and in contributing to the establishment of HCV persistence. This review focuses on recent
studies on how the ISGs response and the IFNλ genetic factors (interleukin-28B and IFNL4) affect
the clinical outcome of HCV infection highlighting their impact in the current antiviral therapies with
direct acting antiviral agents.
Keywords: IFN, ISGs, HCV, IL-28B, IFNL4, DAAs, innate immunity.
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