The Human-Covid Tango: Connecting the Dots

Abstract

As the world grapples with a hot pandemic with various and expanding epicenters, a flurry of medical and scientific activity has gained speed and momentum in a race to halt Covid-19. Due to the urgency of the situation, publication peer review has been speeded up to get information published and turn the gears of research in search for a cure. A hot and controversial topic has been the connection between Covid-19 and the Renin-angiotensin system (RAS). Covid-19, like Sars before it, enters by way of the Angiotensin Converting Enzyme 2 (ACE2). ACE2 is ubiquitously expressed in many tissues in the body serving as the doorway by which the virus can enter and spread causing inflammatory havoc. Demographic evidence coming out of china and other locations make it clear that the elderly and those suffering cardiovascular complications such as hypertension etc are most at risk. The connection to RAS and the demographic nature of the data coming out has led many to advance hypothesis, recommendations and even therapies based on existing RAS inhibitors and other components of the renin-angiotensin system. It is pertinent to review the literature in the context of our understanding of the renin-angiotesnin system to allow better judgements to be made as well as lines of research initiated advancing a quick resolution to Covid-19.

COVID-19 associated complications and potential therapeutic targets

“…The second pathway comprises ACE-2/angiotensin (1-7)/MAS receptors, an anti-growth pathway inhibiting inflammation and promoting vasodilation. Angiotensin 1–7, by binding to the MAS receptor, is known to promote vasodilation, antioxidant, and anti-inflammatory effects ( Hamdi and Abdaldayem, 2020 ; Sriram and Insel, 2020 ). When ACE-2 is activated, angiotensin 1–7 is increased instead of angiotensin II.…”