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

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

1
, 1
 and 1,2,*
Received: 14 June 2009; in revised form: 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.
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 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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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.

AMA Style

Clément S, Pascarella S, Negro F. Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress. Viruses. 2009; 1(2):126-143.

Chicago/Turabian Style

Clément, Sophie; Pascarella, Stéphanie; Negro, Francesco. 2009. "Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress." Viruses 1, no. 2: 126-143.


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