Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel
single-stranded RNA virus and induces cytokines storm that play a
crucial role in the pathogenetic mechanisms of acute respiratory
distress syndrome and the subsequent multi-organ failure. SARS-CoV-2
enters the host cell through angiotensin-converting enzyme 2 (ACE 2)
receptor and patients with forgoing chronic diseases are most vulnerable
to SARS-CoV-2 infection and increase the mortality. ACE 2 is part of the
renin-aldosterone angiotensin system (RAAS) which is highly expressed in
the intestine, pancreas, kidney, heart, lungs, liver, maternal-fetal
interface and fetal tissues. RAAS system is dysregulated in patients
underlying hypertension, cardiovascular diseases, diabetes, renal
disorder and preeclampsia. Drugs acting on the RAAS system,
thiazolidinediones and smoking, preeclampsia, chronic liver diseases
up-regulates the ACE 2 expression that may act as an entry point for
SARS-CoV-2 and leading to multi-organ failure with a massive release of
cytokines. Hence, this review shed a light on a path of increased
mortality rate among COVID-19 patients and the possible mechanism of
multi-organ failure.