Seronello Scott, Sheikh Muhammad Y, Choi Jinah
School of Natural Sciences, University of California at Merced, Merced, CA 95344, USA.
Free Radic Biol Med. 2007 Sep 15;43(6):869-82. doi: 10.1016/j.freeradbiomed.2007.05.036. Epub 2007 Jun 13.
Hepatitis C virus (HCV) is an RNA virus of the Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans, such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV. This review summarizes the current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease.
丙型肝炎病毒（HCV）是黄病毒科的一种RNA病毒，据估计全球有1.7亿人感染该病毒。HCV可导致人类严重的肝脏疾病，如肝硬化、脂肪变性和肝细胞癌。HCV通过多种机制在患者体内诱导氧化/亚硝化应激状态，这种氧化还原紊乱已被认为是HCV诱导发病机制中的关键因素。研究表明，酒精在肝脏疾病的发病机制中与HCV起协同作用，其中部分作用可能由酒精在肝脏代谢过程中产生的活性物质介导。此外，活性物质和酒精可能影响HCV复制及干扰素治疗的效果。饮酒还与HCV RNA序列的序列异质性增加有关，提示酒精与HCV之间存在多种相互作用模式。本综述总结了目前对HCV感染期间氧化和亚硝化应激的认识，以及HCV、酒精和活性物质在肝脏疾病发病机制中可能的联合作用。
