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Molecular Mechanisms Underlying Hepatocellular Carcinoma

HCV Innate Immune Responses

Clinic for Gastroenterology and Hepatology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland
Department of Biomedicine, University Basel, ZLF, Hebelstrasse 20, CH-4031 Basel, Switzerland
Received: 27 August 2009 / Revised: 25 November 2009 / Accepted: 26 November 2009 / Published: 30 November 2009
(This article belongs to the Special Issue Hepatitis Viruses)
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. View Full-Text
Keywords: interferon; MAVS; Toll-like receptors; Jak-STAT; HCV; viral interference interferon; MAVS; Toll-like receptors; Jak-STAT; HCV; viral interference
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MDPI and ACS Style

Heim, M.H. HCV Innate Immune Responses. Viruses 2009, 1, 1073-1088.

AMA Style

Heim MH. HCV Innate Immune Responses. Viruses. 2009; 1(3):1073-1088.

Chicago/Turabian Style

Heim, Markus H. 2009. "HCV Innate Immune Responses" Viruses 1, no. 3: 1073-1088.

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