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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of COVID-19, which has affected more than 6 million people worldwide causing more than 400 000 deaths. The disease affects predominantly the upper and lower respiratory tracts causing severe pulmonary disease which often evolves to a multiorgan systemic disease.1 This is evidenced by thromboembolic lesions of the heart and lungs, pulmonary haemorrhage, muscle weakness, hyperbilirubinaemia and lymphopenia suggesting that COVID-19 affects epithelial barriers, endothelial cells, coagulation, fibrinolysis and the immune system.2 In patients who are severely ill, innate immune hyperactivity causes a cytokine storm which disturbs microcirculation resulting in shock and acute respiratory distress syndrome.3 Systemic disease perpetuation may be due to the virus itself, infecting cells via ACE2 receptor or, following the cytokine storm, due to autoinflammatory and/or autoimmune mechanisms.4
Earlier studies reported that certain autoantibodies such as anti-cardiolipin (a-CL), anti-β2GPI and lupus anticoagulant might associate with the thromboembolic complications occurring …
Handling editor Josef S Smolen
Contributors All authors contributed equally to this work.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.