SARS-CoV-2与宿主固有免疫系统的相互作用

段晓琼; 谢鹤; 陈利民

doi:10.12182/20220160101

SARS-CoV-2与宿主固有免疫系统的相互作用

doi:

段晓琼^1,,
谢鹤^{1, 2},
陈利民^{1, 3, ,}

1. 中国国生物学界科学员工郑州协和生物学界院输液研究分析所（广州 610052）
2. 西电团体诊所（宝鸡 710077）
3. 中国国中医学小学科技术学院静脉注射科学研究院-贵阳中心的血站静脉注射传递的疾病联手试验室室（贵阳 530028）

基金项目: 国家自然科学基金委中德科学中心新冠病毒中德合作应急专项项目（No.C-0029）资助

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通讯作者:
E-mail：limin_chen_99@126.com

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出版历程
- 收稿日期: 2022-09-17
- 修回日期: 2022-11-27
- 网络出版日期: 2023-01-24
- 刊出日期: 2023-01-24

Interaction between SARS-CoV-2 and Host Innate Immunity

1. Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu 610052, China
2. The Hospital of Xidian Group, Xi’an 710077, China
3. Joint Laboratory for Transfusion Transmitted Disease of Nanning Blood Center and Institute of Blood Transfusion of Chinese Academy of Medical Sciences, Nanning 530028, China

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Corresponding author: E-mail: koko体育app:limin_chen_99@126.com

摘要

摘要: 2019冠状病毒病（coronavirus disease 2019, COVID-19，我国通称新型冠状病毒肺炎，简称新冠肺炎）是由严重急性呼吸综合征冠状病毒2（severe acute respiratory syndrome coronavirus 2, SARS-CoV-2）引起的一种以肺部病变为主的呼吸道传染病，自2019年暴发后引起全球性大流行，对公共卫生及民众健康造成严重威胁。Ⅰ型干扰素（interferon, IFN）是宿主固有免疫系统的重要组成部分，在抵御病毒感染过程中发挥着非常重要的作用。病毒和固有免疫系统的博弈，往往决定感染后的疾病进程。研究显示，SARS-CoV-2病毒能通过与宿主免疫系统之间相互作用，抑制IFN的产生及IFN通路的激活；而Ⅰ型IFN反应减弱或延迟，引起宿主免疫应答的紊乱，是造成SARS-CoV-2高发病率和高死亡率的重要原因之一。本文讨论了SARS-CoV-2编码的病毒蛋白与宿主固有免疫系统之间，特别是Ⅰ型IFN通路之间的相互作用，以期为病毒逃逸宿主免疫应答机制及临床上IFN治疗COVID-19提供新思路和新策略。
- 严重急性呼吸综合征冠状病毒2 /
- 病毒蛋白 /
- 干扰素通路 /
- 病毒-宿主相互作用
Abstract: Coronavirus disease 2019 (COVID-19), an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a global pandemic since its outbreak in 2019, presenting serious threats to public health and the health of the people. As one of the main components of the host innate immune system, type-Ⅰ interferon (IFN) plays a critical role in the defense against viral infections. The battle between the virus and the host innate immune system determines the disease progression. It has been reported that SARS-CoV-2 inhibits IFN production and suppresses the activation of IFN signaling pathway through its interactions with the host innate immune system. Then, the weakened or delayed response of type-Ⅰ interferon causes the disturbance of host immune responses, which is one of the important reasons why SARS-CoV-2 causes such high morbidity and mortality. Herein, we reviewed and discussed the interaction between SARS-CoV-2 viral proteins and the host innate immune system, especially the interaction with type-Ⅰ IFN pathway, to provide new insights into the mechanisms of viral evasion of host immune response and new perspectives and strategies for treating COVID-19 with IFN.
- koko体育app: SARS-CoV-2 /
- koko体育app: Viral proteins /
- IFN pathway /
- koko体育app: Virus-host interaction

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图 1 SARS-CoV-2病毒蛋白对Ⅰ型IFN及下游Jak/STAT通路的拮抗作用

Figure 1. The antagonistic effect of SARS-CoV-2 viral protei🔯ns on t𓄧ype-Ⅰ IFN and Jak/STAT pathway
ACE2: Angiotensin converting enzyme 2; TRIM25: Tripartite motif containing 25; CARD: Caspase activation and recruitment domain; RIG-Ⅰ: Retinoic acid-inducible gene-Ⅰ; Nsp: Non-structural protein; MAVS: Mitochondrial antiviral signaling protein; IKKε: IκB kinases ε; TBK1: TANK-binding kinase 1; NF-κB: Nuclear factor kappa-B; IRF: Interferon regulatory factors; ORF: Open reading frame; IFN: Interferon; IFNAR1 and IFNAR2: IFN-alpha/beta receptor 1 and 2; Jak1: Janus kinase-1; Tyk2: Tyrosine kinase 2; STAT1/2: Signal transducer and activator of transcription 1 and 2; ISG15: Interferon-stimulated gene 15; MxA: Human myxovirus resistant protein A; ISRE: Interferon sensitive response element; RNAseL: Ribonuclease L.

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