'L. Spallanzani' National Institute for Infectious Diseases, IRCCS, Italy.
'L. Spallanzani' National Institute for Infectious Diseases, IRCCS, Italy; Department of Biology, 'Tor Vergata' University of Rome, Rome, Italy.
Clin Microbiol Infect. 2016 Oct;22(10):853-861. doi: 10.1016/j.cmi.2016.07.019. Epub 2016 Jul 28.
Hepatitis C virus (HCV) is a major leading cause of hepatocellular carcinoma (HCC). HCV-induced hepatocarcinogenesis is a multistep process resulting from a combination of pathway alterations that are either caused directly by viral factors or immune mediated as a consequence of a chronic state of inflammation. Host genetic variation is now emerging as an additional element that contribute to increase the risk of developing HCC. The advent of direct-acting antiviral agents foresees a rapid decline of HCC rate in HCV patients. However, a full understanding of the HCV-mediated tumourigenic process is required to elucidate if pro-oncogenic signatures may persist after virus clearance, and to identify novel tools for HCC prevention and therapy. In this review, we summarize the current knowledge of the molecular mechanisms responsible for HCV-induced hepatocarcinogenesis.
丙型肝炎病毒 (HCV) 是导致肝细胞癌 (HCC) 的主要原因。HCV 诱导的肝癌发生是一个多步骤的过程,是由病毒因素直接引起或慢性炎症状态下免疫介导的途径改变共同作用的结果。宿主遗传变异现在也成为增加 HCC 发病风险的一个额外因素。直接作用抗病毒药物的出现预计将使 HCV 患者的 HCC 发病率迅速下降。然而,为了阐明病毒清除后是否可能存在致癌特征,以及确定 HCC 预防和治疗的新工具,需要充分了解 HCV 介导的肿瘤发生过程。在这篇综述中,我们总结了导致 HCV 诱导的肝癌发生的分子机制的现有知识。