| Popis: |
Chronic infection with hepatitis C virus (HCV) is characterized by liver inflammation, fibrosis, and hepatocellular carcinoma (HCC). Due to the long delay with which HCC occurs, malignant transformation is thought to be driven by indirect mechanisms. Indeed, HCV is known to create an oxidative microenvironment in the liver, which in turn stimulates repair and regeneration processes. Proliferative repair processes that occur in the context of strong oxidative stress are thought to facilitate fixation and accumulation of genetic mutations and to drive neoplastic transformation. In this review, we summarize knowledge on oxidative stress and oxidative stress responses induced by HCV. We describe the molecular mechanisms by which HCV modulates cellular systems that generate or eliminate oxidative stress and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on HCV replication, as well as the on the course and outcome of liver fibrosis and hepatocarcinogenesis are discussed. |
