丁型肝炎病毒感染的先天免疫识别和调节

StephenW

Innate Immune Recognition and Modulation in Hepatitis D Virus Infection
Stephanie Jung  1 , Sebastian Maximilian Altstetter  1 , Ulrike Protzer  1
Affiliations
Affiliation

    1
    Institute of Virology, Technical University of Munich/Helmholtz Zentrum München, Munich D-81675, Germany.

    PMID: 32550754 PMCID: PMC7284172 DOI: 10.3748/wjg.v26.i21.2781

Abstract

Hepatitis D virus (HDV) is a global health threat with more than 15 million humans affected. Current treatment options are largely unsatisfactory leaving chronically infected humans at high risk to develop liver cirrhosis and hepatocellular carcinoma. HDV is the only human satellite virus known. It encodes only two proteins, and requires Hepatitis B virus (HBV) envelope protein expression for productive virion release and spread of the infection. How HDV could evolve and why HBV was selected as a helper virus remains unknown. Since the discovery of Na+-taurocholate co-transporting polypeptide as the essential uptake receptor for HBV and HDV, we are beginning to understand the interactions of HDV and the immune system. While HBV is mostly regarded a stealth virus, that escapes innate immune recognition, HBV-HDV coinfection is characterized by a strong innate immune response. Cytoplasmic RNA sensor melanoma differentiation antigen 5 has been reported to recognize HDV RNA replication and activate innate immunity. Innate immunity, however, seems not to impair HDV replication while it inhibits HBV. In this review, we describe what is known up-to-date about the interplay between HBV as a helper and HDV's immune evasion strategy and identify where additional research is required.

Keywords: Hepatitis B virus; Hepatitis D virus; Immune evasion; Immunosuppression; Innate immunity; Pathogen-associated molecular pattern molecules.

©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.

StephenW

丁型肝炎病毒感染的先天免疫识别和调节。
斯蒂芬妮·郑1（Stephanie Jung 1，塞巴斯蒂安·马克西米利安·阿尔斯塔特（Sebastian Maximilian Altstetter）1，乌尔里克·普罗策（Ulrike Protzer）1
隶属关系
联系

    1个
    慕尼黑工业大学病毒学研究所/ Helmholtz ZentrumMünchen，慕尼黑D-81675，德国。

    PMID：32550754 PMCID：PMC7284172 DOI：10.3748 / wjg.v26.i21.2781

抽象

丁型肝炎病毒（HDV）是全球健康威胁，超过1500万人受到影响。当前的治疗选择在很大程度上不能令人满意，使长期感染的人处于发展肝硬化和肝细胞癌的高风险中。 HDV是已知的唯一人类卫星病毒。它仅编码两种蛋白质，并且需要表达乙型肝炎病毒（HBV）包膜蛋白才能有效释放和传播感染性病毒粒子。 HDV如何进化以及为何选择HBV作为辅助病毒仍然未知。自从发现Na +-牛磺胆酸盐共转运多肽作为HBV和HDV的必需摄取受体以来，我们开始了解HDV与免疫系统的相互作用。尽管HBV通常被认为是一种隐形病毒，但可以逃避先天免疫识别，而HBV-HDV合并感染的特征是强烈的先天免疫反应。据报道，细胞质RNA传感器黑色素瘤分化抗原5可以识别HDV RNA复制并激活先天免疫。但是，先天免疫力似乎在抑制HBV的同时不会损害HDV复制。在这篇综述中，我们描述了有关作为帮助者的HBV与HDV的免疫逃避策略之间相互作用的最新知识，并确定了需要进行其他研究的地方。

关键词：乙型肝炎病毒；丁型肝炎病毒；免疫逃避；免疫抑制；先天免疫;病原体相关的分子模式分子。

©作者2020。由百世登出版集团有限公司出版。保留所有权利。

StephenW

https://doi.org/10.3748/wjg.v26.i21.2781