COVID-19 (Coronavirus disease 2019) is a public health emergency of international concern. There is a pressing urgency to find treatments based upon currently available scientific knowledge and epidemiological data. In this article, we provide a novel hypothesis describing how the severity of the pathology is mainly resulting from the Antibody responses to SARS-CoV-2 (virus causing COVID-19) and not due to the direct action of the virus. SARS-CoV-2 appears to alter the endothelial cell. The pathophysiological mechanism is not yet elucidated. The damage caused resembles a systemic, multi-organ vasculitis predominantly in the lungs. An increase in thromboembolic complications has been observed in COVID-19 patients. These are manifested by pulmonary embolisms or systemic microembolism manifested by microangiopathy affecting the lungs, brain, liver, kidneys and intestines. Therefore, we hypothesize that an auto-immune acquired Protein S (PS) deficiency may be involved in the pathogenesis of thrombotic events in Covid-19. Auto-antibodies to Protein S may form immune complexes, inducing increased clearance of PS or interfering with the protein C-protein S system. COVID-19 early thromboprophylaxis in infected patients, or even effective anticoagulation, could prevent the progression to severe forms, thus reducing mortality in patients with COVID-19. Activated Protein C (APC), a physiological coagulation inhibitor with cytoprotective properties, could be an interesting avenue for the treatment of severe forms of the disease in intensive care; its administration in hypoxic patients could improve tissue oxygenation. Randomized resuscitation studies in patients with COVID19 are also needed to confirm our hypothesis.
Activated protein C, Anticoagulation, COVID19, Protein S deficiency, Thromboembolic
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