Abstract
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; (b) 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.
Highlights
The emergence of the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has resulted in a rapid response from the global scientific community to better understand its pathophysiology [1,2,3].Despite knowledge gained from SARS-CoV and Middle East respiratory syndrome–coronavirus (MERS-CoV) outbreaks, many aspects of this pandemic are unique to SARS-CoV-2
COVID-19 has a wide spectrum of presentation, ranging from asymptomatic carriers to severe infections resulting in death [4, 5], with 5%–25% of patients requiring ICU-level support [6, 7]
We describe clinical trials that are underway for the treatment of severe COVID-19
Summary
The emergence of the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has resulted in a rapid response from the global scientific community to better understand its pathophysiology [1,2,3].Despite knowledge gained from SARS-CoV and Middle East respiratory syndrome–coronavirus (MERS-CoV) outbreaks, many aspects of this pandemic are unique to SARS-CoV-2. Investigating the temporal nature of the host immune response to SARS-CoV (vis-à-vis complement proteins) will likely provide additional insights and facilitate the personalizing of therapeutics to both promote host defense and minimize tissue injury. In support of this hypothesis, substantially elevated levels of vWF have been identified in patients with severe SARS CoV-2 infection, consistent with endothelial injury [54, 55].
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