1- Inhibition of the coronavirus entrance into the body and
binding to the receptor
SARS-CoV-2 binds to the ACE2 and dysregulates the renin-angiotensin
system (13). SARS-CoV-2 attaches to its receptor using its surface spike
(S) protein (8). Fusion and entrance are based on the binding of the S
protein to the ACE2 receptor on the cells. Due to the ACE2 role as a
viral receptor, there are some suggestions to use AT1R antagonists (ARB)
in COVID-19 treatment (5). Experiments have proved that binding the
coronavirus to its receptors on the cardiac cells, decreased ACE2 enzyme
expression. This action results in ACE enzyme activation and produces
angiotensin. Considering these findings, taking AT1R antagonists seems
to be a suitable option. Although AT1R antagonists have rarely shown
adverse drug reactions But hypotension is reporting in some of the
SARS-CoV patients (13). Both angiotensin converting enzyme inhibitors
(ACEI) and angiotensin II receptor blockers (ARBs) drugs have the same
therapeutic effects and adverse effects; for example: Severe hypotension
after initial doses, acute renal failure (28, 29). Chloroquine was
mentioned to interfere with coronavirus-ACE2 connection. Recombinant
human monoclonal antibodies (mAb) could be used to interfere with virus
binding according to Zhang et al. The mAb could efficiently neutralize
SARS‐CoV and inhibit syncytia formation between cells expressing the S
protein and those expressing the SARS‐CoV receptor ACE2 (8).
Peptide-based vaccines against coronavirus can not be utilized in
subsequent epidemics considering mutations in the virus genome (13).