COVID-19: Acing the Treatment

Abstract

Angiotensin converting enzyme 2 is the functional receptor that the SARS-Cov-2 virus requires to enter cells and cause dysregulated inflammatory conditions that contribute towards acute lung injuries. The renin-angiotensin-aldosterone system with its physiological surveillance and regulation system can be implicated in both harm and therapeutic benefit. The initial observational studies suggesting the discontinuation of angiotensin converting enzyme inhibitors and angiotensin receptor blockers have been firmly rebutted by international societies. On the contrary, these therapeutics may confer a survival benefit in COVID-19 infections. Understanding the biological plausibility of this pathway alongside the emerging therapeutic evidence may yield new modes of treatment. Such developments appear fundamentally important in the battle against the inevitable emergence of new variants and their potential to drive future waves of COVID-19 pandemics.

Keywords: Angiotensin II receptor blockers; Angiotensin converting enzyme inhibitors; COVID-19; Novel treatments; Renin-angiotensin-aldosterone system.

Fig. 1

Positive cellular benefits of the RAAS outnumbering the negative, and how blocking the ACE-Ang II-AT1R coupling may be beneficial. Figure 1 shows the positive cellular benefits of the RAAS outnumbering the negative and how blocking the ACE-Ang II-AT1R coupling may be beneficial. ACE2 usually sits across the cell membrane, but in COVID-19 disease, it is sequestered into the cell rendering it unable to catalyse Ang 1-9 and Ang 1-7 production.