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Viruses 2013, 5(2), 439-469; doi:10.3390/v5020439
Review

HCV and Oxidative Stress in the Liver

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Received: 26 November 2012 / Revised: 26 December 2012 / Accepted: 17 January 2013 / Published: 28 January 2013
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Abstract

Hepatitis C virus (HCV) is the etiological agent accounting for chronic liver disease in approximately 2–3% of the population worldwide. HCV infection often leads to liver fibrosis and cirrhosis, various metabolic alterations including steatosis, insulin and interferon resistance or iron overload, and development of hepatocellular carcinoma or non-Hodgkin lymphoma. Multiple molecular mechanisms that trigger the emergence and development of each of these pathogenic processes have been identified so far. One of these involves marked induction of a reactive oxygen species (ROS) in infected cells leading to oxidative stress. To date, markers of oxidative stress were observed both in chronic hepatitis C patients and in various in vitro systems, including replicons or stable cell lines expressing viral proteins. The search for ROS sources in HCV-infected cells revealed several mechanisms of ROS production and thus a number of cellular proteins have become targets for future studies. Furthermore, during last several years it has been shown that HCV modifies antioxidant defense mechanisms. The aim of this review is to summarize the present state of art in the field and to try to predict directions for future studies.
Keywords: hepatitis C; oxidative stress; Nrf2/ARE pathway; antioxidant defense; iron homeostasis; regulation hepatitis C; oxidative stress; Nrf2/ARE pathway; antioxidant defense; iron homeostasis; regulation
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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Ivanov, A.V.; Bartosch, B.; Smirnova, O.A.; Isaguliants, M.G.; Kochetkov, S.N. HCV and Oxidative Stress in the Liver. Viruses 2013, 5, 439-469.

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