• Abstract
• Full-Text PDF [462 KB]
• Full-Text XML
• Article Versions Notes

• Article Statistics
• PubMed/Medline
• Google Scholar
• Order Reprints

• Cite this article
• Export to BibTeX
• Export to EndNote

• [+] on DOAJ
• Clément, S
• Pascarella, S
• Negro, F
• [+] on Google Scholar
• Clément, S
• Pascarella, S
• Negro, F
• [+] on PubMed
• Clément, S
• Pascarella, S
• Negro, F

•  CiteULike
•  Facebook
•  Mendeley
•  Twitter

This article is

• freely available
• re-usable

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

Review

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

Sophie Clément ¹ , Stéphanie Pascarella ¹  and Francesco Negro ^1,2,*

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; in revised form: 27 July 2009 / Accepted: 29 July 2009 / Published: 11 August 2009

(This article belongs to the Special Issue Hepatitis Viruses)

Download PDF Full-Text [462 KB, uploaded 23 August 2009 16:58 CEST]

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

Article Statistics

Cite This Article