Introduction
The new coronavirus, called SARS-CoV-2, is responsible for the recent outbreak of serious respiratory diseases worldwide. The state of the global pandemic is still being declared and the virus has already claimed thousands of victims. Therapies are urgently needed to contain its rapid spread and reduce high mortality rates, no direct antiviral is yet available and several clinical trials are underway. In addition, no vaccines are currently available and any development in this direction may take several months. Experts in the field have divided SARS-Cov-2 infection into three phases.
Materials and methods
This article explores the scientific hypothesis based on pharmacological and molecular knowledge to consider drugs that modulate the RAS system as therapeutic agents that can help the body fight SARS-CoV-2 infection.
ResultsIt is known from the 2003 SARS epidemic that the critical receptor for SARS-CoV entry into host cells is the angiotensin 2 conversion enzyme (ACE2), the strain involved in the current SARS-CoV-2 epidemic is similar to the SARS-CoV variety involved in the 2002-2003 SARS epidemic. ACE-2 is part of the RAS system, modulating this enzyme could be effective.ConclusionsA scientific hypothesis is described, in the absence of studies and clinical data, based on therapeutic treatments that modulate RAS, and current knowledge of the mechanism of penetration of SARS-CoV-2 into cells, and the role of ACE-2 in the inflammatory state of the infection.SARS-CoV-2
The SARS-Cov-2 virus spread rapidly in several countries, causing a pandemic with thousands of deaths. SARS-Cov-2 is a family of RNA viruses that can infect humans and promote respiratory tract infections and respiratory distress syndrome. Studies have shown that SARS-Cov-2 has about 80% similar genome to the SARS-Cov responsible for the 2003 epidemic. Clinical experts and scientists have described SARS-Cov-2 infection in three phases, the first asymptomatic or slightly symptomatic, the second moderately severe characterized by a pulmonary inflammatory state, the third very severe phase characterized by a generalized inflammatory state affecting all tissues and not only the lungs. Biochemical interaction studies have shown that SARS-Cov-2 uses the ACE-2 receptor protein to penetrate cells. ACE-2 is also a conversion enzyme that is part of the RAS system. To date, there is as yet no conclusive evidence on the role of the RAS system and ACE-2 in the three stages of SARS-Cov-2 infection and, since they are modulated, we know that there are classes of widely used drugs indicated for cardiovascular diseases that can modulate this system, and that have directly or indirectly a potential positive or negative role in the evolution of the disease. (4-5-6)