戊型肝炎病毒感染的免疫发病机制

李晓领; 张青; 王李安; 郑娟娟; 李海

doi:10.3969/j.issn.1001-5256.2022.07.032

戊型肝炎病毒感染的免疫发病机制

DOI: 10.3969/j.issn.1001-5256.2022.07.032

天津市西青医院消化内科，天津 300380

基金项目:

佑安肝病感染病专科医疗联盟科研基金 (LM202019);

天津市西青医院科联体基金项目 (XQYYKLT202006)

利益冲突声明：所有作者均声明不存在利益冲突。

作者贡献声明：李晓领负责资料分析，撰写文章; 张青、王李安、郑娟娟参与收集、分析资料; 李海负责拟定写作思路，指导撰写文章并最后定稿。

详细信息

通信作者:
李海，15202265600@163.com

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出版历程
- 收稿日期: 2021-11-21
- 录用日期: 2022-01-27
- 出版日期: 2022-07-20

Research advances in the immune pathogenesis of hepatitis E virus infection

Department of Gastroenterology and Hepatology, Tianjin Xiqing Hospital, Tianjin 300380, China

Research funding:

Scientific Research Fund of YouAn Medical Alliance for the Liver and Infectious Diseases (LM202019);

The Medical Treatment Combination Fund Project of Tianjin Xiqing Hospital (XQYYKLT202006)

More Information

Corresponding author: LI Hai, 15202265600@163.com (ORCID: 0000-0001-9563-6842)

摘要

摘要: 戊型肝炎大多是急性自限性的，但免疫功能低下患者(如实体器官移植受者、HIV感染和血液疾病)会出现慢性感染。免疫反应是决定戊型肝炎病毒(HEV)感染结局的关键因素，其中包括天然免疫和适应性免疫。通过细胞培养、动物模型和临床试验等多种研究，对HEV免疫发病机制的认识更加深入，这些为HEV新的抗病毒治疗和有效疫苗的开发提供了思路。本综述讨论了近年来有关HEV的免疫发病机制，并提出了对该疾病预防及治疗的展望。
- 戊型肝炎病毒 /
- 病理过程 /
- 适应性免疫 /
- 免疫, 先天
Abstract: Hepatitis E is often acute and self-limited, but immunocompromised patients (such as solid organ transplantation recipients and patients with HIV infection or blood disease) may experience chronic infection. Immune response is the key factor for the outcome of hepatitis E virus (HEV) infection, which includes innate immunity and adaptive immunity. Various studies including cell culture, animal models, and clinical trials have helped to gain a deeper understanding of the immune pathogenesis of HEV, which provided ideas for new antiviral therapies for HEV and the development of effective vaccines. This article reviews the research on the immune pathogenesis of HEV infection in recent years and discusses the prospect of HEV prevention and treatment.
- Hepatitis E Virus /
- Pathologic Processes /
- Adaptive Immunity /
- Immunity, Innate

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图 1 HEV感染与IFN应答的关系

注：病毒感染后，被模式识别受体识别，产生IFN。IFN与其相应受体结合，导致STAT磷酸化，磷酸化的STAT与IRF9形成复合物，易位到细胞核中，通过基因转录，诱导ISG(RIG-1、IRF1、STAT1、STAT2、MDA5)表达，从而抑制病毒复制，这是通常的抗病毒反应。HEV在细胞内的基因及产物也可通过抑制STAT磷酸化等多处信号通路而阻止IFN应答，因此降低IFN抗病毒效应，有利于HEV在人体生存。

Figure 1. Relationship between HEV infection and interferon response

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