Buendia M A
Unité de Recombinaison et Expression Génétique, INSERM U163, Institut Pasteur, Paris, France.
Biomed Pharmacother. 1998;52(1):34-43. doi: 10.1016/s0753-3322(97)86239-7.
Hepatitis B virus (HBV) is a small, enveloped DNA virus which primarily infects liver cells and causes acute and persistent liver disease. Chronic HBV infection, frequently associated with cirrhosis and eventually hepatocellular carcinoma (HCC), represents a major health problem in the world. HBV is the prototype member of the hepadnavirus family, which includes several related mammalian viruses also implicated in liver carcinogenesis in the host. Although epidemiological evidence has clearly linked HBV infection with HCC development, the precise role of the virus and the molecular mechanisms of liver cell transformation remain elusive. Here we discuss potential oncogenic strategies of HBV, ranging from indirect mechanisms related to chronic necroinflammatory disease and to the effects of viral gene products on cell proliferation and apoptosis, to direct insertional activation of cellular (onco)genes. Presently, vaccination of high risk populations represents a major way to prevent the development of HBV-related liver cancer.
乙型肝炎病毒(HBV)是一种小型包膜DNA病毒,主要感染肝细胞并导致急性和持续性肝病。慢性HBV感染常与肝硬化以及最终的肝细胞癌(HCC)相关,是全球主要的健康问题。HBV是嗜肝DNA病毒科的原型成员,该科包括几种相关的哺乳动物病毒,它们在宿主肝脏致癌过程中也有牵连。尽管流行病学证据已明确将HBV感染与HCC发展联系起来,但病毒的确切作用以及肝细胞转化的分子机制仍不清楚。在此,我们讨论HBV潜在的致癌策略,从与慢性坏死性炎症疾病相关的间接机制,到病毒基因产物对细胞增殖和凋亡的影响,再到细胞(癌)基因的直接插入激活。目前,高危人群接种疫苗是预防HBV相关肝癌发生的主要途径。