Hepatitis C Virus Evasion from RIG-I-Dependent Hepatic Innate ImmunityReport as inadecuate




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Gastroenterology Research and PracticeVolume 2010 2010, Article ID 548390, 8 pages

Review ArticleDepartment of Immunology, School of Medicine, University of Washington, Seattle, WA 98195-7650, USA

Received 30 March 2010; Accepted 6 November 2010

Academic Editor: Keigo Machida

Copyright © 2010 Helene Minyi Liu and Michael Gale. 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

Exposure to hepatitis C virus HCV usually results in persistent infection that often develops into chronic liver disease. Interferon-alpha IFN treatment comprises the foundation of current approved therapy for chronic HCV infection but is limited in overall efficacy. IFN is a major effector of innate antiviral immunity and is naturally produced in response to viral infection when viral pathogen-associated molecular patterns PAMPs are recognized as nonself and are bound by cellular pathogen recognition receptors PRRs, including Toll-like receptors TLRs and the RIG-I-like receptors RLRs. Within hepatocytes, RIG-I is a major PRR of HCV infection wherein PAMP interactions serve to trigger intracellular signaling cascades in the infected hepatocyte to drive IFN production and the expression of interferon-stimulated genes ISGs. ISGs function to limit virus replication, modulate the immune system, and to suppress virus spread. However, studies of HCV-host interactions have revealed several mechanisms of innate immune regulation and evasion that feature virus control of PRR signaling and regulation of hepatic innate immune programs that may provide a molecular basis for viral persistence.





Author: Helene Minyi Liu and Michael Gale Jr.

Source: https://www.hindawi.com/



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