Abstract
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.
Resúmen
El primer paso para que el virus SARS-CoV-2 genere alguna alteración en el ser humano es su ingreso. Aunque no es la única forma de transmisión, el principal mecanismo de entrada es por la vía respiratoria. Posteriormente, es necesario que las partículas virales entren en las células para que puedan multiplicarse. Para ingresar a los neumocitos y en general a las células que infecta, el SARS-CoV-2 utiliza como receptor a la enzima convertidora de angiotensina II (ACE2). La célula endocita al virus unido al receptor, y por lo tanto la cantidad de moléculas receptoras (ACE2) disminuyen en la superficie de la célula, de forma que estas moléculas ya no estarán disponibles para llevar a cabo su función, que está relacionada principalmente con la regulación del sistema renina-angiotensina-aldosterona (RAAS). El desequilibrio producido en este sistema puede tener efectos distintos en cada individuo. Los síntomas pueden empeorar aun cuando se ha eliminado la infección, lo que sugiere que parte de la enfermedad se debe a la respuesta del sistema inmune contra las células infectadas. Se desconoce qué es lo que determina la resolución o no de la enfermedad; sin embargo, el estado inicial de salud del paciente parece ser un factor determinante
Ruth Montserrat Rodríguez-Hernández, Universidad Autónoma “Benito Juárez” de Oaxaca, ;
María Coral Rodríguez-Carrasco, CENTRO DE ONCOLOGÍA Y RADIOTERAPIA SERVICIOS DE SALUD DE OAXACA, ;
María de los Angeles Romero-Tlalolini, romerotlalolini@gmail.com , DOCTORADO, CÁTEDRA CONACYT, https://orcid.org/0000-0001-9867-8765 ;
Keywords: SARS-CoV-2, ACE2, neumocitos tipo 2, COVID-19
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(En evaluación)