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    Neuropathogenesis in COVID-19

    Autor: 
    Altable, Marcos
    ;
    De la Serna Tuya, Juan Moisés (1)
    Fecha: 
    11/2020
    Palabra clave: 
    COVID-19; JCR; Scopus
    Tipo de Ítem: 
    other
    URI: 
    https://reunir.unir.net/handle/123456789/11168
    DOI: 
    http://dx.doi.org/10.1093/jnen/nlaa116
    Dirección web: 
    https://academic.oup.com/jnen/article/79/11/1247/5926865
    Open Access
    Resumen:
    SARS-CoV-2 or COVID-19 is a new human coronavirus that emerged in Wuhan, China in late 2019 and is currently causing a pandemic (1, 2). With the possibility of future outbreaks of the disease, it may manifest with diverse clinical characteristics and different severity, as has been seen with other viruses. COVID-19 belongs to a large family of RNA viruses that have been considered a global health problem because they have a remarkably high transmissibility potential and sometimes invade the CNS (3–5). Because of the rapid expansion of a virus that until now was unknown, it is important to understand the mechanisms by which COVID-19 generates CNS disease. Understanding CNS involvement in the disease is especially challenging and current theories of pathogenesis include direct neuroinvasion, crossing of the blood–brain barrier (BBB) by the virus, and a nicotinic hypothesis.
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