Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools

Yajing Fu; Yuanxiong Cheng; Yuntao Wu

doi:10.1007/s12250-020-00207-4

June 2020

Yajing Fu, Yuanxiong Cheng and Yuntao Wu. Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools[J]. Virologica Sinica, 2020, 35(3): 266-271. doi: 10.1007/s12250-020-00207-4

Citation: Yajing Fu, Yuanxiong Cheng, Yuntao Wu. Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools .VIROLOGICA SINICA, 2020, 35(3) : 266-271. http://dx.doi.org/10.1007/s12250-020-00207-4

新型冠状病毒介导的炎症反应--从免疫机制到治疗策略

傅雅静 ^1,2,, ,
程远雄 ³ ,
吴云涛 ^4,,

cstr: 32224.14.s12250-020-00207-4

1.
中国医科大学附属第一医院检验科，国家卫生健康委员会艾滋病免疫学重点实验室(中国医科大学)，辽宁，沈阳，110001
2.
国家临床医学研究中心，中国医科大学附属第一医院，辽宁，沈阳，110001
3.
南方医科大学附属第三医院，呼吸与危重症科，广东，广州，510275
4.
美国乔治梅森大学系统生物学院，弗吉尼亚州，马纳萨斯市，20110

通讯作者： 傅雅静, fufu80s@sina.com, ORCID: http://orcid.org/0000-0002-4343-2220
; 吴云涛, ywu8@gmu.edu, ORCID: http://orcid.org/0000-0002-9547-3278
收稿日期： 2020-02-14
录用日期： 2020-02-16
出版日期： 2020-03-03

摘要

对于新型冠状病毒(SARS-CoV-2)感染造成的严重炎症反应和急性肺损伤，目前尚无有效治疗方法。鉴于SARS-CoV-2与SARS冠状病毒(SARS-CoV)的相似性，我们希望通过对SARS-CoV介导炎症反应机制的探讨，为SARS-CoV-2的临床治疗带来启示。我们认为可以通过抑制Fc受体(FcR)的活化来减少SARS-CoV-2诱导的炎症反应，但临床上目前尚无FcR特异性阻滞剂，因此在处理肺部急性炎症反应时，可以尝试应用免疫球蛋白来封闭Fc受体，避免进一步肺损伤的发生，这种治疗还可与全身性抗炎药物或皮质类固醇联合使用，该疗法的有效性仍需临床验证。

Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools

Yajing Fu ^1,2,, ,
Yuanxiong Cheng ³ ,
Yuntao Wu ^4,,

1.
NHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, the First Affiliated Hospital of China Medical University, Shenyang 110001, China
2.
National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China
3.
Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510275, China
4.
National Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA 20110, USA

Corresponding author: Yajing Fu, fufu80s@sina.com Yuntao Wu, ywu8@gmu.edu
ORCID: http://orcid.org/0000-0002-4343-2220; http://orcid.org/0000-0002-9547-3278
Received Date: 14 February 2020
Accepted Date: 16 February 2020
Published Date: 03 March 2020

Abstract

Currently there is no effective antiviral therapy for SARS-CoV-2 infection, which frequently leads to fatal inflammatory responses and acute lung injury. Here, we discuss the various mechanisms of SARS-CoV-mediated inflammation. We also assume that SARS-CoV-2 likely shares similar inflammatory responses. Potential therapeutic tools to reduce SARS-CoV-2-induced inflammatory responses include various methods to block FcR activation. In the absence of a proven clinical FcR blocker, the use of intravenous immunoglobulin to block FcR activation may be a viable option for the urgent treatment of pulmonary inflammation to prevent severe lung injury. Such treatment may also be combined with systemic anti-inflammatory drugs or corticosteroids. However, these strategies, as proposed here, remain to be clinically tested for effectiveness.
- SARS-CoV-2
- , Inflammatory response
- , Fc receptors (FcR)
- , Antibody-dependent enhancement (ADE)

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