Introduction

Pre-existent cardiovascular disease is a recognized risk factor for COVID-19 infection (1). COVID-19 spike protein uses the angiotensin-converting-enzyme 2 (ACE2) as the binding site to enter the host cell in tongue, bronchi and lungs. Any condition enhancing the expression of ACE2 would increase the vulnerability to infection. Heart failure, coronary artery disease, hypertension, diabetes, ACE inhibitors (ACEi) or angiotensin receptor blockers (ARBs) increase the expression of ACE2, which can be considered nature's endogenous ACE inhibitor at the cellular level. The renin-angiotensin system has 2 arms (Figure, upper panel): the pressor (conventional) arm, composed of Angiotensin II, angiotensin-converting-enzyme (ACE), Angiotensin II-type 1 receptor (AT1R), and the depressor (non conventional) arm consisting of Angiotensin 1-7, ACE2, MAS receptor (MAS R) and Angiotensin II, type 2 receptor (AT2R) (2). The ACE2 (the "good" guy, possibly "the best of enzymes") arm opposes the conventional arm and has beneficial effects in heart failure and acute respiratory distress syndrome (ARDS) (3). COVID-19 spike protein is the "ugly" character in the play. It uses the "good" ACE2 as the binding site. While ACE is detectable in the entire capillary network of the alveoli in the human lung, ACE2 is primarily produced in club cells of distal bronchioles and type 2 pneumocytes in alveolar epithelium. Both cell types are involved in preventing ARDS.

Keywords

Epidemiology

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