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Neuropathogenesis in COVID-19
dc.contributor.author | Altable, Marcos | |
dc.contributor.author | De la Serna Tuya, Juan Moisés | |
dc.date | 2020-11 | |
dc.date.accessioned | 2021-04-05T13:57:37Z | |
dc.date.available | 2021-04-05T13:57:37Z | |
dc.identifier.issn | 1554-6578 | |
dc.identifier.uri | https://reunir.unir.net/handle/123456789/11168 | |
dc.description.abstract | 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. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Journal of Neuropathology & Experimental Neurology | es_ES |
dc.relation.ispartofseries | ;vol. 79, nº 11 | |
dc.relation.uri | https://academic.oup.com/jnen/article/79/11/1247/5926865 | es_ES |
dc.rights | openAccess | es_ES |
dc.subject | COVID-19 | es_ES |
dc.subject | JCR | es_ES |
dc.subject | Scopus | es_ES |
dc.title | Neuropathogenesis in COVID-19 | es_ES |
dc.type | other | es_ES |
reunir.tag | ~ARI | es_ES |
dc.identifier.doi | http://dx.doi.org/10.1093/jnen/nlaa116 |
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