PROS1 and COVID-19: Patients with COVID-19 have severe endothelial damage in their lungs, including viral invasion and rupture of the endothelial cell membrane.109 Another study identified the co-presence of SARS-CoV-2 N protein and ACE2 receptor on the pulmonary vascular endothelium in postmortem COVID-19 patient samples.110 Moreover, IFN-α or -β can promote SARS-CoV-2 pulmonary vascular infection by inducing the expression of ACE2 in human primary lung endothelial cells.111 S1 and S2 subunits of S protein mediate attachment and membrane fusion, respectively.