Figure 2.

This central illustration schematically illustrates our proposed mechanism of viral endothelial injury. The virus may infect the endothelial cell and monocytes, leading to cytopathic effects, increasing levels of cytotoxins including interleukin 6 (il-6) and tumor necrosis factor α (tnf alpha), and cytokine dysregulation, and cause platelet activation and alterations in platelet binding, vascular permeability, endothelial platelet interactions that may in turn cause widespread endothelial dysfunction, cytokine storm, heightened immune response, and multiorgan system involvement and potentially failure. NET, neutrophil extracellular trap; PMN, polymorphonuclear; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TF, tissue factor; VE, vascular endothelial; VWF, von Willebrand factor.