ACE2 and severe acute respiratory syndrome: Downregulation of ACE2 and the binding of the spike protein of this receptor contribute to lung injury during SARS, resulting in the excessive production of angiotensin II, stimulating the type 1a angiotensin II receptor (AGRT1A), increasing the pulmonary vascular permeability and explaining the increased lung pathology, with decreased expression of ACE2 [11].