Fig. 1

Pathophysiology. a Viral entrance: ACE2 and DPP4. The coronavirus entrance in cells is facilitated by its spike protein using ACE2. b Endothelial cell damage and thromboinflammation. ACE2-mediated entry of SARS-CoV-2 in endothelial cells induce inflammation and the generation of a prothrombotic milieu, and results in increased thrombin production associated with inhibition of fibrinolysis and activation of complement pathways, a cascade which will lead to microthrombi deposition. The cross-talk between platelets and neutrophils and the activation of macrophages has an important role in the proinflammatory effects, characterized by cytokine release, the formation of neutrophil extracellular traps (NETs), and microthrombus deposition. c Dysregulation of the immune response. Dysregulation of the immune response of COVID-19, in which there is an increase in cytokine release associated with an attenuation of interferon response