Lung histological analyses revealed the presence of vascular inflammation and severe endothelial injury as a direct consequence of intracellular severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and ensuing host inflammatory response in coronavirus disease 2019 (COVID-19).1 Endothelial cells promote coagulation following injury, leading to widespread formation of microthrombi, provoking microcirculatory failure or large-vessel thrombosis.2 Growing evidence suggests that microvascular thrombosis is a major pathophysiological event in COVID-19 pathogenesis. Damaged endothelial cells could be closely implicated in the prothrombotic state commonly reported in severe patients in the intensive care unit (ICU). How SARS-CoV-2 exerts its cytopathic effects is still a matter of debate, and ultrastructural evidence of direct viral replication in endothelial cells remains to be demonstrated. Although direct viral tissue damage is a plausible mechanism of injury,3 endothelial damage and thromboinflammation associated with dysregulated immune responses, inducing microvascular thrombosis, represent an attractive alternative hypothesis.2 Using cultured human pulmonary microvascular endothelial cells (HPMVEC), we assessed whether plasma collected from patients with COVID-19 at different disease stages could trigger endothelial damage in vitro.

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