COVID-19: ACE2centric infective disease?

Diffuse pulmonary inflammation, endothelial inflammation and enhanced thrombosis are cardinal features of COVID-19, the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). These features are reminiscent of several adverse reactions triggered by angiotensin II, and opposed by angiotensin1-7, in many experimental models. SARS-CoV-2 binds to ACE2 receptors and entries into the cell through the fusion of its membrane with that of the cell. Hence, it down-regulates these receptors. The loss of ACE2 receptor activity from the external site of the membrane will lead to less angiotensin II inactivation and less generation of antiotensin1-7. In various experimental models of lung injury, the imbalance between angiotensin II over-activity and of antiotensin1-7 deficiency triggered inflammation, thrombosis and other adverse reactions. In COVID-19, such imbalance could play an important role in influencing the clinical picture and outcome of the disease. According to this line of thinking, some therapeutic approaches including recombinant ACE2, exogenous angiotensin1-7 and angiotensin receptor blockers appear particularly promising and are being actively tested.