Herzer K, Sprinzl M F, Galle Peter R
Deptartment I of Internal Medicine, Mainz University, Mainz, Germany.
Liver Int. 2007 Apr;27(3):293-301. doi: 10.1111/j.1478-3231.2006.01422.x.
Viral hepatitis is a diffuse inflammatory reaction of the liver caused by hepatotropic viruses. Among the hepatitis viruses, only hepatitis B virus and hepatitis C virus are able to persist in the host and cause chronic hepatitis. In the course of persistent infection, inflammation forms the pathogenetic basis of chronic hepatitis that can lead to nodular fibrosis, which can progress to cirrhosis and, eventually, hepatocellular carcinoma (HCC). Of the different antiviral defense systems employed by the host, apoptosis significantly contributes to the prevention of viral replication, dissemination, and persistence. Pathomorphologic studies have shown acidophilic bodies and hepatocyte dropout, features that are compatible with apoptosis. The number of hepatocytes showing features of apoptosis in patients with chronic hepatitis B and C was found to be higher than in healthy subjects, indicating that apoptosis is involved in the pathogenesis of these diseases. There are various data suggesting that hepatitis B and C viral proteins may modulate apoptosis. Vice versa, mechanisms of apoptosis inhibition might represent central survival strategies employed by the virus which, in the end, may contribute to HCC development. While the expression and retention of viral proteins in hepatocytes may influence the severity and progression of liver disease, the mechanisms of liver injury in viral hepatitis are defined to be due not only to the direct cytopathic effects of viruses, but also to the host immune response to viral proteins expressed by infected hepatocytes. However, the exact role of these observations in relation to pathogenesis remains to be established. The mechanism and systems are complex. This report aims to provide an overview and intends to cite only a small number of pertinent references.
病毒性肝炎是由嗜肝病毒引起的肝脏弥漫性炎症反应。在肝炎病毒中，只有乙型肝炎病毒和丙型肝炎病毒能够在宿主体内持续存在并导致慢性肝炎。在持续感染过程中，炎症形成慢性肝炎的发病基础，可导致结节性纤维化，进而发展为肝硬化，并最终发展为肝细胞癌（HCC）。在宿主采用的不同抗病毒防御系统中，细胞凋亡对预防病毒复制、传播和持续存在有显著作用。病理形态学研究显示了嗜酸性小体和肝细胞脱落，这些特征与细胞凋亡相符。发现慢性乙型和丙型肝炎患者中表现出细胞凋亡特征的肝细胞数量高于健康受试者，这表明细胞凋亡参与了这些疾病的发病机制。有各种数据表明，乙型和丙型肝炎病毒蛋白可能调节细胞凋亡。反之，细胞凋亡抑制机制可能代表病毒采用的核心生存策略，最终可能促成肝细胞癌的发展。虽然病毒蛋白在肝细胞中的表达和保留可能影响肝病的严重程度和进展，但病毒性肝炎肝损伤的机制不仅被定义为病毒的直接细胞病变效应，还包括宿主对受感染肝细胞表达的病毒蛋白的免疫反应。然而，这些观察结果在发病机制方面的确切作用仍有待确定。其机制和系统很复杂。本报告旨在提供一个概述，仅引用少量相关参考文献。
