乙型肝炎管理的当前最佳实践和了解治愈的长期前景

StephenW

乙型肝炎管理的当前最佳实践和了解治愈的长期前景
David Yardeni 1 , Kyong-Mi Chang 2 , Marc G Ghany 3
隶属关系
隶属关系

    1
    美国国立卫生研究院糖尿病、消化和肾脏疾病研究所肝病科，贝塞斯达，马里兰州；临床肝病研究员，肝病分部，国家糖尿病和消化和肾脏疾病研究所，美国国立卫生研究院，大厦。 10, Room 4-5722, 10 Center Drive, MSC 1800, Bethesda, MD 20892-1800。电子地址：[email protected]。
    2
    宾夕法尼亚大学佩雷​​尔曼医学院医学研究，下士 Michael J. Crescenz VA 医学中心和医学系，宾夕法尼亚州费城；副参谋长兼研究副院长，Michael J. Crescenz VA 下士医学中心和宾夕法尼亚大学佩雷​​尔曼医学院医学教授，宾夕法尼亚州费城，19104。电子地址：[email protected]。
    3
    美国国立卫生研究院糖尿病、消化和肾脏疾病研究所肝病科，贝塞斯达，马里兰州；美国国立卫生研究院国家糖尿病、消化和肾脏疾病研究所肝病分部高级研究员，Bldg 10, Room 9B-16, 10 Center Drive, MSC 1800, Bethesda, MD 20892-1800。电子地址：[email protected]。

    PMID：36243037 DOI：10.1053/j.gastro.2022.10.008

抽象的

乙型肝炎病毒 (HBV) 是全球肝硬化和肝细胞癌的主要原因。尽管疫苗有效，但慢性感染的流行率仍然很高。目前的疗法在实现治疗中但不是治疗后病毒抑制方面是有效的。乙型肝炎表面抗原 (HBsAg) 的丧失是治疗后病毒抑制的最佳替代标志物，与改善的临床结果相关。不幸的是，目前的治疗很少能达到这个终点，因为它们对共价闭合环状 DNA（病毒转录和基因组复制的模板）缺乏影响。我们对 HBV 病毒学的理解取得了重大进展，同时对免疫发病机制有了更好的理解，导致开发了许多新的治疗方法，有望实现功能性治愈（HBsAg 消失），甚至可能完全治愈（清除 cccDNA 和整合的 HBV DNA） .本综述将涵盖当前管理慢性 HBV 感染的最佳实践和新兴的 HBV 感染新疗法及其治愈前景。

版权所有 © 2022 AGA 研究所。由 Elsevier Inc. 出版。保留所有权利。

StephenW

Current Best Practice in Hepatitis B Management & Understanding Long-Term Prospects for Cure
David Yardeni  1 , Kyong-Mi Chang  2 , Marc G Ghany  3
Affiliations
Affiliations

    1
    Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD; Clinical Liver Diseases Fellow, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10, Room 4-5722, 10 Center Drive, MSC 1800, Bethesda, MD 20892-1800. Electronic address: [email protected].
    2
    Medical Research, Corporal Michael J. Crescenz VA Medical Center & Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA; Associate Chief of Staff and Associate Dean for Research, Corporal Michael J. Crescenz VA Medical Center and Professor of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104. Electronic address: [email protected].
    3
    Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD; Senior Investigator, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg 10, Room 9B-16, 10 Center Drive, MSC 1800, Bethesda, MD 20892-1800. Electronic address: [email protected].

    PMID: 36243037 DOI: 10.1053/j.gastro.2022.10.008

Abstract

The hepatitis B virus (HBV) is a major cause of cirrhosis and hepatocellular carcinoma worldwide. Despite an effective vaccine the prevalence of chronic infection remains high. Current therapy is effective at achieving on-treatment but not off-treatment viral suppression. Loss of hepatitis B surface antigen (HBsAg), the best surrogate marker of off-treatment viral suppression, is associated with improved clinical outcomes. Unfortunately, this endpoint is rarely achieved with current therapy because of their lack of effect on covalently closed circular DNA, the template of viral transcription and genome replication. Major advancements in our understanding of HBV virology along with better understanding of immunopathogenesis have led to the development of a multitude of novel therapeutic approaches with the prospect of achieving functional cure (HBsAg loss) and perhaps complete cure (clearance of cccDNA and integrated HBV DNA). This review will cover current best practice for managing chronic HBV infection and emerging novel therapies for HBV infection and their prospect for cure.

Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.