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.
Highlights
Hepatitis C virus (HCV) is a human pathogen, which accounts for approximately 3–4 million new cases of viral hepatitis each year [1]
This review aims to summarize current data on how HCV modulates and controls formation and eradication of reactive oxygen species (ROS) and the potential roles of HCV induced ROS in the emergence and development of the various pathologies associated with chronic disease (CHC)
HCV genome translation is another step in the viral replication cycle which has been shown to be affected by oxidative stress
Summary
Hepatitis C virus (HCV) is a human pathogen, which accounts for approximately 3–4 million new cases of viral hepatitis each year [1]. Studies investigating the underlying mechanisms suggest that oxidative stress plays a central role in all these pathologies These data will be summarized in the current review below. Eukaryotic cells possess a special system of defense against oxidative stress [12,13] It is comprised of low molecular weight compounds (glutathione and other antioxidants) and “phase II defense enzymes” capable of scavenging ROS. ROS induce cellular stress either via their direct interaction with various biological molecules including nucleic acids, proteins, and lipids or via activation of classical signaling cascades that regulate stress responses. This review aims to summarize current data on how HCV modulates and controls formation and eradication of ROS and the potential roles of HCV induced ROS in the emergence and development of the various pathologies associated with CHC.
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