ACE2 and acute respiratory distress syndrome: Studies have shown that SARS-CoV-2 enters the host cells by binding to ACE-2 and subsequently impedes the breakdown of bradykinin and its mediators.[39] This is thought to cause overstimulation of the bradykinin pathway, resulting in increased vascular leakage and angioedema.[40] These postulated mechanisms are comparable to those in acute respiratory distress syndrome, where the virus triggers acute pulmonary edema.