Local Complement Contributes to Pathogenic Activation of Lung Endothelial Cells in SARS-CoV-2 Infection

This study investigated the role of endothelial dysfunction and inflammation in the vascular pathology of COVID-19. While the evidence does not suggest direct infection of endothelial cells by SARS-CoV-2, inflammatory responses seem to result from epithelial cell infection. The researchers found that lung vascular cells had significantly lower expression of ACE2 and TMPRSS2, making them less susceptible to productive viral infection. However, these cells showed abortive infection when exposed to a SARS-CoV-2-conditioned medium. Additionally, under hypoxic conditions, exposure to the conditioned medium led to the upregulation of inflammatory factors and complement components, contributing to lung endothelial and vascular dysfunction during COVID-19.