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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 9012580, 13 pages
Review Article

HCV and Oxidative Stress: Implications for HCV Life Cycle and HCV-Associated Pathogenesis

1Department of Virology, Paul-Ehrlich-Institut, Paul-Ehrlich-Straße 51–59, 63225 Langen, Germany
2Deutsches Zentrum für Infektionsforschung (DZIF), Gießen-Marburg-Langen, 63225 Langen, Germany

Received 25 November 2015; Accepted 14 January 2016

Academic Editor: Alexander V. Ivanov

Copyright © 2016 Regina Medvedev et al. 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.


HCV (hepatitis C virus) is a member of the Flaviviridae family that contains a single-stranded positive-sense RNA genome of approximately 9600 bases. HCV is a major causative agent for chronic liver diseases such as steatosis, fibrosis, cirrhosis, and hepatocellular carcinoma which are caused by multifactorial processes. Elevated levels of reactive oxygen species (ROS) are considered as a major factor contributing to HCV-associated pathogenesis. This review summarizes the mechanisms involved in formation of ROS in HCV replicating cells and describes the interference of HCV with ROS detoxifying systems. The relevance of ROS for HCV-associated pathogenesis is reviewed with a focus on the interference of elevated ROS levels with processes controlling liver regeneration. The overview about the impact of ROS for the viral life cycle is focused on the relevance of autophagy for the HCV life cycle and the crosstalk between HCV, elevated ROS levels, and the induction of autophagy.