Hino O
Nihon Rinsho. 1993 Feb;51(2):531-5.
Persistent hepatitis B virus (HBV) infection is epidemiologically closely associated with the development of human hepatocellular carcinoma (HCC). A molecular mechanism that would explain the strong epidemiological link of persistent HBV infection with HCCs is still open to debate. Among HBV carriers, HCC develops only in patients with chronic liver disease, such as chronic active hepatitis, liver fibrosis, or liver cirrhosis. In other words, hepatitis-related proliferative changes, which are mainly sustained by repeating cycles of cell death and regeneration either immunologically or through virus infection, appear important for HBV hepatocarcinogenesis. The same mechanism may also be present in human hepatitis C virus-related hepatocarcinogenesis. In this article, I reviewed animal models of HBV-related hepatocarcinogenesis. It is important to evaluate and check whether the animal models are fit with human HBV hepatocarcinogenesis or not.
持续性乙型肝炎病毒（HBV）感染在流行病学上与人类肝细胞癌（HCC）的发生密切相关。一种能够解释持续性HBV感染与HCC之间紧密流行病学联系的分子机制仍存在争议。在HBV携带者中，HCC仅发生于患有慢性肝病的患者，如慢性活动性肝炎、肝纤维化或肝硬化。换句话说，主要通过免疫或病毒感染反复经历细胞死亡和再生循环而维持的肝炎相关增殖性变化，对于HBV肝癌发生似乎很重要。相同的机制可能也存在于人类丙型肝炎病毒相关的肝癌发生中。在本文中，我回顾了HBV相关肝癌发生的动物模型。评估和检查动物模型是否符合人类HBV肝癌发生情况很重要。
