Department of Virology, Paul-Ehrlich-Institut, Paul-Ehrlich-Straβe 51-59, D-63225 Langen, Germany.
Int J Mol Sci. 2019 Sep 19;20(18):4659. doi: 10.3390/ijms20184659.
With respect to their genome and their structure, the human hepatitis B virus (HBV) and hepatitis C virus (HCV) are complete different viruses. However, both viruses can cause an acute and chronic infection of the liver that is associated with liver inflammation (hepatitis). For both viruses chronic infection can lead to fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Reactive oxygen species (ROS) play a central role in a variety of chronic inflammatory diseases. In light of this, this review summarizes the impact of both viruses on ROS-generating and ROS-inactivating mechanisms. The focus is on the effect of both viruses on the transcription factor Nrf2 (nuclear factor erythroid 2 (NF-E2)-related factor 2). By binding to its target sequence, the antioxidant response element (ARE), Nrf2 triggers the expression of a variety of cytoprotective genes including ROS-detoxifying enzymes. The review summarizes the literature about the pathways for the modulation of Nrf2 that are deregulated by HBV and HCV and describes the impact of Nrf2 deregulation on the viral life cycle of the respective viruses and the virus-associated pathogenesis.
就其基因组和结构而言，乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV）是完全不同的病毒。然而，这两种病毒都可引起肝脏的急性和慢性感染，导致肝脏炎症（肝炎）。对于这两种病毒，慢性感染可导致纤维化、肝硬化和肝细胞癌（HCC）。活性氧（ROS）在各种慢性炎症性疾病中起核心作用。有鉴于此，本综述总结了这两种病毒对产生 ROS 和灭活 ROS 的机制的影响。重点是这两种病毒对转录因子 Nrf2（红系细胞衍生 2 型（NF-E2）相关因子 2）的影响。Nrf2 通过与其靶序列抗氧化反应元件（ARE）结合，触发多种细胞保护基因的表达，包括 ROS 解毒酶。该综述总结了关于 HBV 和 HCV 调节 Nrf2 的途径的文献，并描述了 Nrf2 失调对各自病毒的病毒生命周期和与病毒相关的发病机制的影响。
