The Ineluctable Role of ACE-2 Receptors in SARS COV-2 Infection and Drug Repurposing as a Plausible SARS COV-2 Therapy: A Concise Treatise

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent for the COVID-19 infectious disease that spreads via the respiratory route and has reached a drastic level of a global pandemic. Symptoms of COVID-19 may vary from mild (fever, dry cough, shortness of breath) to severe pneumonia-like respiratory symptoms as exacerbation of disease occurs. Unlike SARS-CoV, the SARSCoV- 2 has a higher binding affinity to ACE-2 receptors, which signifies its higher transmission rate from person to person. Even though ACE-2 is significant in the reninangiotensin- aldosterone system (RAAS) regulation that exhibits protection to various organs, it plays a significant role in COVID-19 disease pathogenesis. Viral interferences with the ACE-2 peptidase activity are found in SARS-CoV-2 infected patients leading to pro-inflammatory responses, hypertension and multi-organ damage. Angiotensinconverting enzyme-2 is constrained to a variety of organ systems, but surface ACE-2 receptors on lung epithelia are largely affected, which lead to pathological alterations in lung histology which may progress to respiratory failure. The viral tropism mainly occurs by the attachment to the angiotensin-converting enzymes-2 receptors in the host cell; thus drugs targeting ACE-2 expressions may arise as the future therapeutic strategy to combat COVID-19 infections. The innovative approach of repurposing drugs has shown temporary effectiveness to curb the rising pandemic. This article mainly focuses on the prominence of ACE-2 receptors which are expressed during the COVID infections and the repurposing strategy of available drug therapies.