乙型肝炎病毒前核心/核心启动子突变及其与基因型和肝病严

StephenW

乙型肝炎病毒前核心/核心启动子突变及其与基因型和肝病严重程度的相关性综述
拉杰什库马尔 1
隶属关系
联系

    1
    哈里亚纳邦政府学校教育部，Panchkula 134109，哈里亚纳邦，印度。 [email protected]。

    PMID：35646275 PMCID：PMC9099108 DOI：10.4254/wjh.v14.i4.708

抽象的

全世界有 3.5 亿人长期感染乙型肝炎病毒 (HBV)，并且在以后的生活中面临发展为肝硬化和肝细胞癌 (HCC) 的风险。 HBV是最多样化的DNA病毒，其基因组由四个开放阅读框组成：前表面抗原/表面抗原基因（preS/S）、前核心/核心基因（preC/C）、聚合酶基因（P）和X基因（X）。由于在逆转录过程中缺乏校对活动和高复制率，HBV 会自然产生准种或响应抗病毒剂产生准种。该病毒有 10 种基因型（A 到 J），具有不同的地理分布。 HBV基因组中存在多种HBV突变，包括preC/C突变、preS/S突变、P基因突变和X基因突变。核心启动子区域在病毒的复制、形态发生和发病机制中起着至关重要的作用。前核心区域在病毒复制中也起着至关重要的作用。核心启动子和前核心突变都将病毒从宿主免疫监视中拯救出来，并导致形成可能改变致病性的突变株。 preC/C 突变与肝病进展有关。前核心突变停止乙型肝炎 e 抗原 (HBeAg) 的产生，基础核心启动子突变下调 HBeAg 的产生。基础核心启动子的突变也与 HBV 复制增加和晚期肝病如肝硬化和 HCC 的发病率增加有关。抗病毒耐药突变的出现是治疗失败的主要原因。本综述主要关注 preC/C 启动子突变及其与基因型和肝病严重程度的相关性。对 HBV 遗传多样性和突变体的全面认识和了解对于发现 HBV 感染的预后和控制技术至关重要。

关键词：急性肝炎；基础核心启动子；核心启动子区；暴发性肝炎;乙型肝炎病毒;乙型肝炎病毒e抗原；肝细胞癌;前核区。

©作者 2022。由百视登出版集团有限公司出版。保留所有权利。

StephenW

Review on hepatitis B virus precore/core promoter mutations and their correlation with genotypes and liver disease severity
Rajesh Kumar  1
Affiliations
Affiliation

    1
    Department of School Education, Haryana Government, Panchkula 134109, Haryana, India. [email protected].

    PMID: 35646275 PMCID: PMC9099108 DOI: 10.4254/wjh.v14.i4.708

Abstract

Of 350 million people worldwide are chronically infected with hepatitis B virus (HBV) and are at risk of developing cirrhosis and hepatocellular carcinoma (HCC) later in life. HBV is the most diverse DNA virus, and its genome is composed of four open reading frames: Presurface antigen/surface antigen gene (preS/S), precore/core gene (preC/C), polymerase gene (P), and the X gene (X). HBV produces quasispecies naturally or in response to antiviral agents because of the absence of proofreading activity amid reverse transcription and a high replication rate. The virus has 10 genotypes (A to J) with different geographical distributions. There are various HBV mutations in the HBV genome, including preC/C mutations, preS/S mutations, P gene mutations, and X gene mutations. The core promoter region plays a vital part in the replication, morphogenesis and pathogenesis of the virus. The precore region also plays a crucial role in viral replication. Both core promoter and precore mutations rescue the virus from host immune surveillance and result in the formation of mutated strains that may have altered pathogenicity. preC/C mutations are associated with liver disease progression. Precore mutations stop hepatitis B e antigen (HBeAg) production and basal core promoter mutations downregulate HBeAg production. Mutations in the basal core promoter are also associated with increased HBV replication and an increased incidence of advanced liver diseases such as cirrhosis and HCC. The emergence of antiviral-resistant mutations is the main reason for treatment failure. This review focuses mainly on preC/C promoter mutations and their correlation with genotypes and liver disease severity. Thorough perception and knowledge of HBV genetic variety and mutants could be vital to discover techniques for the prognosis and control of HBV infection.

Keywords: Acute hepatitis; Basal core promoter; Core promoter region; Fulminant hepatitis; Hepatitis B virus; Hepatitis B virus e antigen; Hepatocellular carcinoma; Precore region.

©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

StephenW

https://doi.org/10.4254/wjh.v14.i4.708