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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
世界华人消化杂志. 2015-10-18; 23(29): 4658-4664
在线出版日期: 2015-10-18. doi: 10.11569/wcjd.v23.i29.4658
HBV DNA整合与慢性乙型肝炎、原发性肝癌关系研究进展
吴殿磊, 徐光华, 刘娜
吴殿磊, 西藏民族大学附属医院感染病科 陕西省咸阳市 712082
吴殿磊, 徐光华, 刘娜, 延安大学附属医院感染病科 陕西省延安市 716000
吴殿磊, 讲师, 副主任医师, 博士, 主要从事慢性乙型肝炎的研究.
基金项目: 国家自然科学基金资助项目, No. 81560102.
作者贡献分布: 本文由徐光华构思审校; 吴殿磊与刘娜收集资料; 论文写作由吴殿磊完成.
通讯作者: 徐光华, 教授, 主任医师, 硕士生导师, 716000, 陕西省延安市中心街250号, 延安大学附属医院感染病科. wudianlei@163.com
电话: 0911-2881196
收稿日期: 2015-08-27
修回日期: 2015-09-15
接受日期: 2015-09-21
在线出版日期: 2015-10-18

乙型肝炎病毒(hepatitis B virus, HBV)是导致慢性肝炎的主要病因, 同时也是原发性肝细胞癌的主要危险因素之一, 研究证实HBV可以通过整合自身基因进入到宿主基因组中或者通过其结构蛋白、分泌蛋白, 或者通过表观遗传导致宿主基因突变, 突变主要包括, 肝细胞部分DNA缺失和染色体重排等. HBV DNA整合对病毒本身和宿主肝细胞可以产生影响, 有些突变与慢性乙型肝炎(chronic hepatitis B, CHB)和终末期肝病[肝硬化、原发性肝癌(primary liver cancer, PLC)]有关. 我们总结归纳该领域HBV DNA整合方面的主要研究成果予以综述. 期望为乙型肝炎慢性化机制研究以及PLC基因诊断和治疗提供新的思路和线索.

关键词: 乙型肝炎病毒DNA; 整合; 原发性肝癌; 慢性乙型肝炎; 整合位点鉴定
引文著录: 吴殿磊, 徐光华, 刘娜. HBV DNA整合与慢性乙型肝炎、原发性肝癌关系研究进展. 世界华人消化杂志 2015; 23(29): 4658-4664
Association of integration of HBV DNA into host genome with CHB and PLC
Dian-Lei Wu, Guang-Hua Xu, Na Liu
Dian-Lei Wu, Department of Infectious Diseases, the Affiliated Hospital of Xizang Minzu University, Xianyang 712082, Shaanxi Province, China
Dian-Lei Wu, Guang-Hua Xu, Na Liu, Department of Infectious Diseases, the Affiliated Hospital of Yan'an University, Yan'an 716000, Shaanxi Province, China
Supported by: National Natural Science Foundation of China, No. 81560102.
Correspondence to: Guang-Hua Xu, Professor, Chief Physician, Department of Infectious Diseases, the Affiliated Hospital of Yan'an University, 250 Zhongxin Street, Yan'an 716000, Shaanxi Province, China. wudianlei@163.com
Received: August 27, 2015
Revised: September 15, 2015
Accepted: September 21, 2015
Published online: October 18, 2015

Hepatitis B virus (HBV) is the main cause of chronic hepatitis B (CHB) and one of the major risk factors for primary liver cancer (PLC). A study has proved that HBV has some mutagenic effects on the host genome. HBV may be exhibiting these mutagenic effects through integrating into the host genome, through its viral proteins (structural protein or secreted proteins) or through some epigenetic mechanisms related with HBV proteins. The mutations mainly include loss of partial liver cell DNA and chromosome rearrangement. HBV DNA integration can influence the virus itself and the host cells, and some mutations of HBV DNA are associated with end-stage liver disease [e.g., hepatocellular carcinoma (PLC)] and chronic hepatitis B. This review summarizes the progress in research of HBV DNA integration to provide a new thought or clue for the study of the mechanism of chronic hepatitis B, and PLC diagnosis and treatment.

Key Words: Hepatitis B virus DNA; Integration; Primary liver cancer; Chronic hepatitis B; Integration site
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