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Open Access Highly Accessed Review

Oxidative stress and hepatitis C virus

Usman Zafar Paracha1, Kaneez Fatima2, Mohammad Alqahtani3, Adeel Chaudhary35, Adel Abuzenadah45, Ghazi Damanhouri5 and Ishtiaq Qadri5*

Author Affiliations

1 Department of Pharmaceutics, Hajvery University, Lahore, Pakistan

2 IQ Institute of Infection and Immunity, Lahore, Punjab, Pakistan

3 Center of Excellence in Genomic Medicine, King Abdul Aziz University, PO Box 80216, Jeddah, 21589, Saudi Arabia

4 Faculty of Applied Medical Sciences, King Abdulaziz University, PO Box 80216, Jeddah 21589, Saudi Arabia

5 King Fahd Medical Research Center, King Abdul Aziz University, PO Box 80216, Jeddah 21589, Saudi Arabia

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Virology Journal 2013, 10:251  doi:10.1186/1743-422X-10-251

Published: 7 August 2013

Abstract

The disproportionate imbalance between the systemic manifestation of reactive oxygen species and body’s ability to detoxify the reactive intermediates is referred to as oxidative stress. Several biological processes as well as infectious agents, physiological or environmental stress, and perturbed antioxidant response can promote oxidative stress. Oxidative stress usually happens when cells are exposed to more electrically charged reactive oxygen species (ROS) such as H2O2 or O2-. The cells’ ability to handle such pro-oxidant species is impeded by viral infections particularly within liver that plays an important role in metabolism and detoxification of harmful substances. During liver diseases (such as hepatocellular or cholestatic problems), the produced ROS are involved in transcriptional activation of a large number of cytokines and growth factors, and continued production of ROS and Reactive Nitrogen Species (RNS) feed into the vicious cycle. Many human viruses like HCV are evolved to manipulate this delicate pro- and antioxidant balance; thus generating the sustainable oxidative stress that not only causes hepatic damage but also stimulates the processes to reduce treatment of damage. In this review article, the oxidant and antioxidant pathways that are perturbed by HCV genes are discussed. In the first line of risk, the pathways of lipid metabolism present a clear danger in accumulation of viral induced ROS. Viral infection leads to decrease in cellular concentrations of glutathione (GSH) resulting in oxidation of important components of cells such as proteins, DNA and lipids as well as double strand breakage of DNA. These disorders have the tendency to lead the cells toward cirrhosis and hepatocellular carcinoma in adults due to constant insult. We have highlighted the importance of such pathways and revealed differences in the extent of oxidative stress caused by HCV infection.

Keywords:
Oxidative stress; ROS; HCV