乙型肝炎病毒持续感染和先天免疫缺陷：细胞相关或病毒相

StephenW

World J Clin Cases. 2018 Sep 6;6(9):233-241. doi: 10.12998/wjcc.v6.i9.233.
Hepatitis B virus-persistent infection and innate immunity defect: Cell-related or virus-related?
Tang J1, Wu ZY1, Dai RJ2, Ma J1, Gong GZ3.
Author information

1
    Department of Infectious Disease, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.
2
    Department of Infectious Disease, the First Affiliated Hospital of University of South China, Hengyang 421001, Hunan Province, China.
3
    Department of Infectious Disease, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China. [email protected].

Abstract

The outcomes of hepatitis B virus (HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be self-limited, in contrast to perinatal acquirement, for which chronic persistence of the HBV is a general outcome. Innate immunity plays an indispensable role in early virus infection, facilitating virus clearance. However, it has been reported that HBV is under-recognized and poorly eliminated by the innate immune system in the early stages of infection, possibly explaining the long-lasting persistence of viremia afterwards. Furthermore, due to the existence of covalently closed circular DNA, chronic HBV clearance is very difficult, even when patients are given interferon-α and nucleotide/nucleoside analogs for antiviral therapy. The mechanism by which HBV evades innate immune recognition and establishes persistent infection remains a subject of debate. Besides, some researchers are becoming more interested in how to eradicate chronic HBV infection by restoring or boosting innate immunity. This review aimed to summarize the current knowledge on how intrahepatocyte signaling pathways and innate immune cells act after the onset of HBV infection and how these actions are related to the persistence of HBV. We anticipate the insights presented herein to be helpful for future development of novel immune therapeutic strategies to fight HBV infection.
KEYWORDS:

Dendritic cells; Hepatitis B virus; Immune evasion; Innate immunity; Kupffer cells; Natural killer cells; Pattern recognition receptor; Toll-like receptor

PMID:
    30211203
PMCID:
    PMC6134278
DOI:
    10.12998/wjcc.v6.i9.233

StephenW

世界J Clin案件。 2018年9月6日; 6（9）：233-241。 doi：10.12998 / wjcc.v6.i9.233。
乙型肝炎病毒持续感染和先天免疫缺陷：细胞相关或病毒相关？
Tang J1，Wu ZY1，Dai RJ2，Ma J1，Gong GZ3。
作者信息

1
    中南大学湘雅二医院传染病科，湖南长沙410011
2
    南华大学第一附属医院传染病科，湖南衡阳421001
3
    中南大学湘雅二医院传染病科，湖南长沙410011 [email protected]。

抽象

乙型肝炎病毒（HBV）感染的结果与获得感染的年龄密切相关。与围产期获得相比，成人生活中获得的感染往往是自限性的，对于这种感染，HBV的慢性持续性是一般结果。先天免疫在早期病毒感染中起着不可或缺的作用，促进病毒清除。然而，据报道，在感染的早期阶段，HBV被先天免疫系统认识不足并且很少被消除，这可能解释了之后病毒血症的长期持续存在。此外，由于存在共价闭合的环状DNA，即使给予患者干扰素-α和核苷酸/核苷类似物用于抗病毒治疗，慢性HBV清除也是非常困难的。 HBV逃避先天免疫识别并建立持续感染的机制仍然是一个争论的主题。此外，一些研究人员对如何通过恢复或增强先天免疫来消除慢性HBV感染更感兴趣。本综述旨在总结目前关于肝细胞信号通路和先天免疫细胞如何在HBV感染发病后起作用以及这些作用如何与HBV持续存在相关的知识。我们预计本文提供的见解有助于未来开发针对HBV感染的新型免疫治疗策略。
关键词：

树突状细胞;乙型肝炎病毒;免疫逃避;先天免疫;库普弗细胞;自然杀手细胞;模式识别受体; Toll样受体

结论：
    30211203
PMCID：
    PMC6134278
DOI：
    10.12998 / wjcc.v6.i9.233