Elucidating the neuropathologic mechanisms of SARS-cov-2 infection.
Fecha
2021-04-12Autor
Pacheco Herrero, Mar
Soto Rojas, Luis O.
Harrington, Charles R.
Flores Martínez, Yazmín M.
Villegas Rojas, Marcos M.
León Aguilar, Alfredo M.
Martínez Gómez, Paola A.
Campa Córdoba, B. Berenice
Apátiga Pérez, Ricardo
Corniel Taveras, Carolin N.
Domínguez García, Jesabelle de J.
Blanco Alvarez, Víctor Manuel
Luna Muñoz, José
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The current pandemic caused by the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a public health emergency. To date, March 1, 2021, coronavirus disease 2019 (COVID-19) has caused about 114 million accumulated cases and 2.53 million deaths worldwide. Previous pieces of evidence suggest that SARS-CoV-2 may affect the central nervous system (CNS) and cause neurological symptoms in COVID-19 patients. It is also known that angiotensin-converting enzyme-2 (ACE2), the primary receptor for SARS-CoV-2 infection, is expressed in different brain areas and cell types. Thus, it is hypothesized that infection by this virus could generate or exacerbate neuropathological alterations. However, the molecular mechanisms that link COVID-19 disease and nerve damage are unclear. In this review, we describe the routes of SARS-CoV-2 invasion into the central nervous system. We also analyze the neuropathologic mechanisms underlying this viral infection, and their potential relationship with the neurological manifestations described in patients with COVID-19, and the appearance or exacerbation of some neurodegenerative diseases.
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