Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.
Nat Rev Immunol
; 21(5): 319-329, 2021 05.
Article
in English
| MEDLINE | ID: covidwho-1171402
ABSTRACT
Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Venous Thrombosis
/
Cytokine Release Syndrome
/
COVID-19
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Nat Rev Immunol
Journal subject:
Allergy and Immunology
Year:
2021
Document Type:
Article
Affiliation country:
S41577-021-00536-9
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