Pathophysiology of multi-organ damage in SARS-CoV-2 infection

Tiburcio López-Pérez, Gerardo Patricia Ramírez-Sandoval María de Lourdes Solyenetzin Torres-Altamirano Mayra; Tiburcio Lopez-Perez, Gerardo; Patricia Ramirez-Sandoval, Maria de Lourdes; Solyenetzin Torres-Altamirano, Mayra

SARS-CoV-2 could originate from unknown bats or intermediate hosts and cross the species barrier to humans. Virus-host interactions affect viral entry and replication. The virus genome encodes four essential structural proteins, the spike glycoprotein, the small envelope protein, the matrix proteins, and the nucleocapsid protein. The SARSCoV- 2 glycoprotein S binds to the host cell receptors of the enzyme, the conversion of angiotensin 2 (ACE2), which is a critical step for virus entry. It is expressed more in men than in women, probably by estradiol and testosterone that can influence ACE activity in different ways. In the viremia phase, it passes from the salivary glands and mucous membranes, especially the nasal and larynx, to the lungs and other organs with the same ACE2 receptors, such as the heart, liver, and even the central nervous system. It can reach the intestines, which can explain the symptoms and is detected in the stool from the beginning of the infection. Comorbidities such as immunodeficient status, old age, systemic arterial hypertension, diabetes mellitus or chronic lung diseases, obesity or smoking are key to viral pathogenesis. When the immune system is inefficient to effectively control the virus in the acute phase, it can evolve into a macrophage activation syndrome that results in the dreaded cytokine storm that puts the patient in a very critical condition. Understanding the pathophysiology of SARS-CoV-2 infection is the cornerstone to provide timely diagnosis and implement appropriate treatment for patients, limiting the spread of the virus and ultimately eliminating the presence of the virus in humanity. (English) [ABSTRACT FROM AUTHOR] La glucoproteína S del SARS-CoV-2 se une a la enzima convertidora de la angiotensina 2 (ACE2). El genoma del virus codifica cuatro proteínas estructurales esenciales: glucoproteína espiga, proteína de envoltura pequeña, proteínas matrices y proteína de nucleocápside. Se expresa más en hombres, quizá por el estradiol y la testosterona. En la viremia pasa de las glándulas salivales y membranas mucosas, especialmente nasal y laringe, a los pulmones y a otros órganos con los mismos receptores ACE2: corazón, hígado e, incluso, al sistema nervioso central;llega a los intestinos, lo que puede explicar los síntomas ;se detecta en las heces desde el inicio de la infección. La coexistencia de hipertensión arterial sistémica, diabetes mellitus o neumopatías crónicas, obesidad o tabaquismo, inmunodeficiencias y la senescencia son clave en la patogénesis viral. Cuando el sistema inmunológico es ineficiente en controlar efectivamente al virus en la fase aguda, puede evolucionar a un síndrome de activación de macrófagos que da pie a la temida tormenta de citocinas que pone al paciente en un estado crítico. Entender la fisiopatogenia de la infección por SARS-CoV-2 es la piedra angular para establecer el diagnóstico oportuno e implementar el tratamiento adecuado y limitar la propagación del virus y, en última instancia, eliminarlo. (Spanish) [ABSTRACT FROM AUTHOR] Copyright of Acta Pediatrica de Mexico is the property of Instituto Nacional de Pediatria (INP) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)