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dc.contributor.authorAltable, Marcos
dc.contributor.authorDe la Serna Tuya, Juan Moisés
dc.date2020-11
dc.date.accessioned2021-04-05T13:57:37Z
dc.date.available2021-04-05T13:57:37Z
dc.identifier.issn1554-6578
dc.identifier.urihttps://reunir.unir.net/handle/123456789/11168
dc.description.abstractSARS-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.isoenges_ES
dc.publisherJournal of Neuropathology & Experimental Neurologyes_ES
dc.relation.ispartofseries;vol. 79, nº 11
dc.relation.urihttps://academic.oup.com/jnen/article/79/11/1247/5926865es_ES
dc.rightsopenAccesses_ES
dc.subjectCOVID-19es_ES
dc.subjectJCRes_ES
dc.subjectScopuses_ES
dc.titleNeuropathogenesis in COVID-19es_ES
dc.typeotheres_ES
reunir.tag~ARIes_ES
dc.identifier.doihttp://dx.doi.org/10.1093/jnen/nlaa116


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