Almost a year ago, I remember seeing this post here about how ACE inhibitors and ARBs may increase the risk of severe COVID-19:
It turns out, after many large observational studies, including metanalysis of these studies, that these drugs do not increase risk and decrease risk in some circumstances:
https://www.medrxiv.org/content/10.1101/2020.05.03.20089375v1
Two randomized controlled trials that suspended ACEi/ARBs in COVID-19 positive hospitalized patients such as BRACE Corona (https://pubmed.ncbi.nlm.nih.gov/33464336/) showed again no delirious impact of RAS inhibitors in the context of COVID-19 hospitalization.
Mounting in vitro and in vivo data supports the theory that these drugs may, if dosed appropriately, help in the context of COVID-19 - e.g. ARBs may be a viable treatment.
For instance, this animal study establishes a causal link between the renin-angiotensin system and COVID-19:
https://www.researchsquare.com/article/rs-124634/v1
In the above animal study, it’s shown that the ACE2 enzyme activity itself (not as a receptor) modulates the severity of lung damage. While ARBs do not directly affect the ACE2 receptor, they likely work to stop this lung damage in a similar way (see https://www.nature.com/articles/nm1267 - for SARS, where losartan performs as well as soluble ACE2 in attenuating lung injury).
I’ve already typed too much (!) but the page above is a good catalog of these trials (de novo invitation of ARBs / renin-angiotensin modulating drugs in the context fo COVID-19)