乙型肝炎病毒变异与肝细胞癌发生关系  

Mutations of Hepatitis B Virus and Hepatocellular Carcinoma

作　　者：朱冬梅[1] 周乙华[1,2] 

机构地区：[1]南京大学医学院附属鼓楼医院感染科,南京市210008 [2]江苏省医学分子技术重点实验室,南京市210008

出　　处：《医学分子生物学杂志》2011年第1期84-88,共5页Journal of Medical Molecular Biology

基　　金：江苏省医学重点人才项目（No.RC2007005）

摘　　要：乙型肝炎病毒（hepatitisBvirus，HBV）基因组复制时，以病毒前基因组RNA作为模板合成子代病毒DNA，催化该过程的逆转录酶缺乏校对功能，所以HBV易出现变异。近年来，各国学者通过比较肝细胞癌（hepatocellular carcinoma，HCC）患者和非HCC患者的HBV基因序列，发现HBV基本核心启动子区的A1762T／G1764A变异或T1753V变异、增强子Ⅰ区的G1053A或G1229A变异、前S蛋白的F141L变异、前s2区基因缺失变异和x基因的截短变异，分别是HCC的易患因素，而前c区常见的G1896A变异，与HCC的发生无关。增强子Ⅱ区的C1653T变异在c基因HBV感染中可能与发生HCC有关，而在A基因型可能无关。Hepatitis B virus （HBV） is prone to undergo genetic mutations, since HBV replicates its progeny DNA through reverse transcription of pregenomic RNA, which is intermediated by the viral polymerase that lacks proofreading activity. Recently, comparison of HBV sequences derived from hepatocellular carcinoma （HCC） and non-HCC patients infected with HBV has revealed the increased mutations in the basal core promoter （A1762T/G1764A or T1753V） and enhancer I （G1053A or G1229A） , F141L mutation in pre-S protein, deletion in the pre-S2 gene, and the C- terminal deletion of X gene, which may lead to the risk of HCC development. G1896A mutation in the pre-C gene is not associated with HCC. Mutation in enhancer Ⅱ （C1653T） in HBV genotype C, but not in genotype A, appears as a potential risk factor for HCC.

关 键 词：乙型肝炎病毒 基因变异 肝细胞癌 

分 类 号：R512.6[医药卫生—内科学]