ACE 2 inhibitors and ARBs:
SARS-CoV-2 binds through ACE 2 receptors found predominantly in the
lungs and enters the cells. In a case report, infecting Vero E6 cells
with SARS and concomitantly giving human recombinant soluble ACE2 ( hrs
ACE 2) to check the inhibitory effects of this drug on the viral entry
into the cell. The infection is markedly reduced, and similar
observations are obtained by infecting human capillary organoids and
kidney organoids. In a prospective study, induced myocardial infarction
in rats, which was chronically managed by ATR1 blockers, shows
upregulation of cardiac ACE2 receptors. 13Also, kidney
ACE 2 receptors were upregulated in rat studies after this treatment. In
humans, this is confirmed by raised urinary ACE 2 levels. Viral entry is
responsible for the downregulation of ACE 2 receptors, thereby
increasing angiotensin responsible for lung injury. Although this seems
paradoxical, ATR1 blockers are therapeutically exploited to prevent
acute lung injury. [14]In another randomized
clinical trial, confirmed COVID-19 patients (n=500) are treated with ACE
2 inhibitor and ATR1 blockers, and their hospital-stay and disease
progression is assessed. This treatment is effective in decreasing the
mortality rate as compared to those not taking these drugs.[37]
Colchicine:
In uncontrolled case series, COVID patients (n=9) are treated with
colchicine, and the safety of the drug is assessed. Symptoms among most
of the patients improved. Early administration of this drug is not
beneficial as it impairs the immune response, and it is not effective in
the later stages due to organ dysfunctioning by the cytokine
storm[53]. There are four ongoing pieces of
research on colchicine, which mainly address the topic of losing dose
effectiveness in controlling myocardial complications, the response in
patients with severe infection, efficacy in pneumonia, and reduction in
death rate as a result of short-term treatment with this medicine.[36]