Hepatitis C Virus, Oxidative Stress and Steatosis: Current Status and Perspectives

J.      Gonzalez-Gallego; M.      V. Garcia-Mediavilla; S.      Sanchez-Campos

doi:10.2174/156652411795976592

Abstract

Reactive oxygen and nitrogen species (ROS/RNS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment. When the production of ROS/RNS overrides the antioxidant capability of the target cells, oxidative damage may occur as a consequence of the interaction with DNA, protein, and lipids. Hepatitis C virus (HCV) is a major cause of viral hepatitis. Although the molecular mechanisms of HCV pathogenesis remain unclear, oxidative stress is emerging as a key step and a major initiator in the development and the progression of liver damage, and the evaluation of oxidative stress may be useful for a better understanding of the pathogenesis of hepatitis C. Liver steatosis is one of the most important histopathological features in patients with chronic hepatitis C. Both viral and host factors contribute to the development of steatosis, and putative defects caused by ROS/RNS may be involved through abnormalities in lipid metabolism. This review is aimed to offer an updated overview of the relationship between oxidative stress and HCV infection, focusing on the significance of ROS/RNS in the pathogenesis of liver disease. The potential role played by oxidative stress in the pathogenic mechanisms of HCV-related steatosis is also discussed.

Keywords: Calcium, core protein, hepatitis C virus, insulin resistance, NS5A protein, oxidative stress, replication, steatosis, infection, inflammation, hepatocellular carcinoma, aerobic environment, cytotoxicity, peroxynitrite, serological markers