Elucidating the neuropathologic mechanisms of SARS-CoV-2 infection

Mar Pacheco-Herrero, Luis O Soto-Rojas, Charles Harrington, Yazmin M. Flores Martinez, Marcos M Villegas-Rojas, Alfredo M. León-Aguilar, Paola A Martínez-Gómez, B. Berenice Campa-Córdoba, Ricardo Apátiga-Pérez, Carolin N. Corniel-Taveras, Jesabelle de J. Dominguez-García, Victor Manuel Blanco-Alvarez, José Luna-Muñoz* (Corresponding Author)

*Corresponding author for this work

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28 Citations (Scopus)
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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.
Original languageEnglish
Article number660087
Number of pages19
JournalFrontiers in Neurology
Early online date12 Apr 2021
Publication statusPublished - 12 Apr 2021


  • SARS-CoV-2
  • storm cytokine syndrome
  • neuroinflammation
  • blood-brain barrier
  • neurological alterations
  • Alzheimer’s disease


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