Complement and coagulation: key triggers of COVID-19-induced multiorgan pathology.
J Clin Invest
; 130(11): 5674-5676, 2020 11 02.
Article
in English
| MEDLINE | ID: covidwho-760323
ABSTRACT
In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Peptides, Cyclic
/
Pneumonia, Viral
/
Thromboplastin
/
Coronavirus Infections
/
Complement Activation
/
Thrombotic Microangiopathies
/
Pandemics
/
Betacoronavirus
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
J Clin Invest
Year:
2020
Document Type:
Article
Affiliation country:
Jci142780
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