Overview of hepatitis B viral replication and genetic variability.

Overview of hepatitis B viral replication and genetic variability.
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DOI:
10.1016/j.jhep.2016.01.027
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发表时间:
2016-04
影响因子:
25.7
通讯作者:
Revill P
Revill P
中科院分区:
医学1区
文献类型:
--
作者:
Tong S;Revill P

文献摘要

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慢性感染B型肝炎病毒(HBV)会大大增加肝硬化和肝细胞癌(HCC)的风险。世界范围内的HBV分离株可分为10种基因型。此外,免疫清除阶段选择病毒基因组不同部分的突变。HBV感染的结果是由传播方式、宿主遗传因素、病毒基因型和适应性突变以及环境因素的复杂相互作用形成的。核心启动子突变和消除HBeAg表达的突变与急性肝功能衰竭有关,而基因型B、C、A1亚型、核心启动子突变、preS缺失、包膜蛋白C端截短和剪接的前基因组RNA与HCC的发生有关。我们治疗和预防HBV感染的努力受到了耐药突变体和疫苗逃逸突变体的阻碍。本文概述了乙型肝炎病毒的生命周期,然后从生物学特性和临床意义方面综述了乙型肝炎病毒基因型和突变体。
Chronic infection with hepatitis B virus (HBV) greatly increases the risk for liver cirrhosis and hepatocellular carcinoma (HCC). HBV isolates worldwide can be divided into 10 genotypes. Moreover, the immune clearance phase selects for mutations in different parts of the viral genome. The outcome of HBV infection is shaped by the complex interplay of the mode of transmission, host genetic factors, viral genotype and adaptive mutations, as well as environmental factors. Core promoter mutations and mutations abolishing HBeAg expression have been implicated in acute liver failure, while genotypes B, C, subgenotype A1, core promoter mutations, preS deletions, C-terminal truncation of envelope proteins, and spliced pregenomic RNA are associated with HCC development. Our efforts to treat and prevent HBV infection are hampered by the emergence of drug resistant mutants and vaccine escape mutants. This paper provides an overview of the HBV life cycle, followed by review of HBV genotypes and mutants in terms of their biological properties and clinical significance.