Abstract

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.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call