乙型肝炎病毒持续感染致癌过程中的相关问题  

Persistent hepatitis B virus infection in the development of hepatocellular carcinoma:recent progresses

作　　者：侯晓玫[1] 曹广文[1] 

机构地区：[1]第二军医大学流行病学教研室,上海200433

出　　处：《中国病毒病杂志》2014年第3期230-234,共5页Chinese Journal of Viral Diseases

基　　金：国家自然科学基金重大研究计划项目(91129301);国家自然科学基金国家杰出青年科学基金(81025015)

摘　　要：肝癌是全球最常见的恶性肿瘤之一,有较高的致死率。2008年全球肝癌新发病例约748 300例,死亡病例约695 900例。其中我国大陆地区新发肝癌患者和死于肝癌患者数量均占全球50%左右[1]。原发性肝癌有70%~85%为肝细胞癌（HCC）,其中85%以上是由乙型肝炎（乙肝）病毒（HBV）慢性感染所致[2]。HBV感染已成为我国重大公共卫生问题。HBV基因全长大约为3.2×103 bp,Hepatocellular carcinoma （HCC）, the second cause of cancer-related death in China's Mainland, is mainly caused by chronic hepatitis B virus （HBV） infection. Genetic predisposition of human leukocyte anti- gen class Ⅱ contributes to the maintenance of chronic HBV infection. Nonresolving inflammation resulted from the interaction of HBV and the host immune system is essential for the evolution of HBV and subsequent HCC occurrence. Persistent and insufficient antiviral immunity positively selects HBV mutants. During the inflamma- tion-driven carcinogenesis, the genomes of both HBV and hepatocyte experience an evolutionary process of ＂mutation-selection-adaptation＂ . HBV mutations not only predict but also promote the development of HCC. The integration of HBV genome, especially in a form of the carboxylic-terminal truncated HBV X protein, not only promotes HCC occurrence and metastasis, but also confers the resistance to antiviral treatments.

关 键 词：乙型肝炎病毒突变 免疫 肝细胞癌 

分 类 号：R373.2[医药卫生—病原生物学]