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Viruses 2009, 1(3), 1073-1088; doi:10.3390/v1031073
HCV Innate Immune Responses
Received: 27 August 2009; in revised form: 25 November 2009 / Accepted: 26 November 2009 / Published: 30 November 2009
(This article belongs to the Special Issue Hepatitis Viruses)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: Hepatitis C virus (HCV) establishes a persistent infection in more than 70% of infected individuals. This striking ability to evade the powerful innate immune system results from viral interference occurring at several levels of the interferon (IFN) system. There is strong evidence from cell culture experiments that HCV can inhibit the induction of IFNβ by cleaving important proteins in the virus sensory pathways of cells such as MAVS and TRIF. There is also evidence that HCV interferes with IFNα signaling through the Jak-STAT pathway, and that HCV proteins target IFN effector systems such as protein kinase R (PKR). These in vitro findings will have to be confirmed in clinical trials investigating the molecular mechanisms of HCV interference with the innate immune system in liver samples.
Keywords: interferon; MAVS; Toll-like receptors; Jak-STAT; HCV; viral interference