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Viruses 2009, 1(2), 126-143; doi:10.3390/v1020126

Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress

1
Division of Clinical Pathology, University Hospitals, Geneva, Switzerland
2
Division of Gastroenterology and Hepatology, University Hospitals, Geneva, Switzerland
*
Author to whom correspondence should be addressed.
Received: 14 June 2009 / Revised: 27 July 2009 / Accepted: 29 July 2009 / Published: 11 August 2009
(This article belongs to the Special Issue Hepatitis Viruses)
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Abstract

The persistent infection with hepatitis C virus is a major cause of chronic liver disease worldwide. However, the morbidity associated with hepatitis C virus widely varies and depends on several host-related cofactors, such as age, gender, alcohol consumption, body weight, and co-infections. The objective of this review is to discuss three of these cofactors: steatosis, insulin resistance and oxidative stress. Although all may occur independently of HCV, a direct role of HCV infection in their pathogenesis has been reported. This review summarizes the current understanding and potential molecular pathways by which HCV contributes to their development. View Full-Text
Keywords: hepatitis C; reactive oxygen species; insulin signaling; lipid accumulation hepatitis C; reactive oxygen species; insulin signaling; lipid accumulation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Clément, S.; Pascarella, S.; Negro, F. Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress. Viruses 2009, 1, 126-143.

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