Open AccessCÓMO NOS ENFERMA EL SARS-CoV-2?
Author(s) -
Ruth Montserrat Rodríguez-Hernández,
María Coral Rodríguez-Carrasco,
María de los Ángeles Romero-Tlalolini
Publication year - 2020
Publication title -
ra rió guendaruyubi
Language(s) - English
Resource type - Journals
eISSN - 2594-0562
pISSN - 2594-0554
DOI - 10.53331/rar.v3i9.6675
Subject(s) - receptor , renin–angiotensin system , immune system , virus , biology , cell , microbiology and biotechnology , viral entry , virology , immunology , endocrinology , viral replication , genetics , blood pressure
The first step for the SARS-CoV-2 virus to generate any alteration in humans is its entry. Although it is not the only form of transmission, the main mechanism of entry is through the respiratory route. Subsequently, it is necessary for the viral particles to enter the cells so that they can multiply. To enter pneumocytes and, in general, the cells it infects, SARS-CoV-2 uses angiotensin-converting enzyme II (ACE2) as a receptor. The cell endocytes the virus bound to the receptor, and therefore the amount of receptor molecules (ACE2) decreases on the cell surface, so that these molecules will no longer be available to carry out their function, which is mainly related to the regulation of the renin-angiotensin-aldosterone system (RAAS). The imbalance produced in this system may have different effects in each individual. Symptoms may worsen even when the infection has been eliminated, suggesting that part of the disease is due to the immune system response against infected cells. It is not known what determines whether the disease resolves or not; however, the patient's initial state of health appears to be a determining factor.