The complement system in COVID-19: friend and foe?

被引：265

作者：

Java, Anuja ^{[1
]}

Apicelli, Anthony J. ^{[2
]}

Liszewski, M. Kathryn ^{[3
]}

Coler-Reilly, Ariella ^{[3
]}

Atkinson, John P. ^{[1
]}

Kim, Alfred H. J. ^{[3
]}

Kulkarni, Hrishikesh S. ^{[4
]}

机构：

[1] Washington Univ, Sch Med, Div Nephrol, St Louis, MO USA

[2] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO USA

[3] Washington Univ, Sch Med, Dept Med, Div Rheumatol, 660 S Euclid Ave,Campus Box 8045, St Louis, MO 63110 USA

[4] Washington Univ, Sch Med, Dept Med, Div Pulm & Crit Care Med, 4523 Clayton Ave,Campus Box 8052, St Louis, MO 63110 USA

来源：

JCI INSIGHT | 2020年 / 5卷 / 15期

关键词：

CORONAVIRUS DISEASE 2019; INTRACELLULAR COMPLEMENT; CLINICAL CHARACTERISTICS; BLOOD-GROUP; CROSS-TALK; ACTIVATION; PROTEINS; C5A; INFECTION; ANTIBODY;

D O I：

10.1172/jci.insight.140711

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Coronavirus disease 2019 (COVID-19), the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has resulted in a global pandemic and a disruptive health crisis. COVID-19-related morbidity and mortality have been attributed to an exaggerated immune response. The role of complement activation and its contribution to illness severity is being increasingly recognized. Here, we summarize current knowledge about the interaction of coronaviruses with the complement system. We posit that (a) coronaviruses activate multiple complement pathways; (h) severe COVID-19 clinical features often resemble complementopathies; (c) the combined effects of complement activation, dysregulated neutrophilia, endothelial injury, and hypercoagulability appear to be intertwined to drive the severe features of COVID-19; (d) a subset of patients with COVID-19 may have a genetic predisposition associated with complement dysregulation; and (e) these observations create a basis for clinical trials of complement inhibitors in life-threatening illness.

引用

页数：13

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