Feitelson M A
Fox Chase Cancer Center, Philadelphia, PA 19111.
Mol Biol Med. 1989 Oct;6(5):367-93.
The pathogenesis of hepatitis B virus (HBV) infection is variable and can result in the development of acute and chronic hepatitis, cirrhosis and primary hepatocellular carcinoma (PHC). In this review, the relationship between the patterns of virus gene expression, host immunological responses, and liver pathology in chronic infection will be discussed. Available evidence suggests that the virus is not directly cytopathic to liver cells and that the pathologic sequelae to infection are mediated by both humoral and cellular immune responses against one or more virus gene products. In addition, chronic liver disease might also be mediated by autoaggressive immune responses that may be stimulated by the direct action of virus gene products upon host gene expression, by the lysis of infected hepatocytes by virus specific host immune responses, or by both. Given the complex and variable outcome of HBV infection, the lack of adequate treatment for chronic liver disease, and the fact that long-term infection dramatically increases the risk of developing PHC, the future provides challenges for devising new models to study, understand and successfully manipulate the pathogenesis of chronic HBV infection.
乙型肝炎病毒（HBV）感染的发病机制具有多样性，可导致急性和慢性肝炎、肝硬化及原发性肝细胞癌（PHC）的发生。在本综述中，将讨论慢性感染中病毒基因表达模式、宿主免疫反应和肝脏病理之间的关系。现有证据表明，该病毒对肝细胞并无直接细胞病变作用，感染的病理后遗症是由针对一种或多种病毒基因产物的体液免疫和细胞免疫反应介导的。此外，慢性肝病也可能由自身攻击性免疫反应介导，这种反应可能是由病毒基因产物对宿主基因表达的直接作用、病毒特异性宿主免疫反应对受感染肝细胞的裂解作用或两者共同作用所刺激。鉴于HBV感染的结果复杂多变、慢性肝病缺乏足够的治疗方法，以及长期感染会显著增加发生PHC的风险，未来在设计新模型以研究、理解并成功控制慢性HBV感染的发病机制方面面临着挑战。
