Figure 1.

Pulmonary epithelial & endothelial damage, platelet activation and coagulopathy in COVID-19. (A) On the left, the normal alveolar and endothelial interface is depicted; the right side highlights the pathophysiology of severe SARS-CoV-2 infection in the lung which includes infection, inflammation, activation of endothelial, platelet and coagulation pathways, and alveolar oedema. (B) The virus infects and damages the pulmonary epithelial and endothelial cells, initiating a cascade of events such as endothelial activation—release of proinflammatory and prothrombotic factors (such as von Willebrand factor (VWF), thrombin and thrombomodulin), platelet hyperactivation—platelet micro vesicle and granule release of (P-selectin, beta thromboglobulin) into circulation and coagulation activation—increased clot formation leading to fibrinolysis and increased fibrin degradation products and D-Dimer.