Angiotensin-Converting Enzymes, the Key Components in the Pathogenesis of COVID-19 Infection and their Role in the Interaction of SARS-Cov-2 with Human Host Cells

Over the past 20 years, seven coronaviruses have caused more or less severe respiratory diseases in humans. Among these, the most important ones are SARS-CoV and the coronavirus, a similar virus that has created a pandemic called Covid-19 since 2019, belonging to the b-category of beta-coronaviruses called Sarbecovirus.This virus is due to a kind of spike-like structure to the ACE2 receptor (angiotensin converting enzyme 2) bind to the surface of host cells. Often, dysfunction of ACE2 protease after viral infection leads to dysfunction of the RAAS (renin-angiotensin-aldosterone) pathway and, as a result, by affecting blood pressure, it upsets the balance of fluids and electrolytes in the body, a process that results in increased inflammation and permeability of arteries in the airways. Furthermore, the widespread release of cytokines by the immune cells in response to viral and/or secondary infections can lead to cytokine storms along with symptoms of sepsis. In these cases, uncontrolled inflammation causes multiple organ damage that leads to organ failure, particularly in cardiovascular, hepatic, and renal systems.

Despite the findings of the pathogenic mechanism of SARS-CoV-2, there is still no specific drug to treat COVID-19. Therefore, achieving proper therapeutic strategies against COVID-19 requires a comprehensive understanding of its pathogenesis in the host for developing new drugs and/or using approved drugs.