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Does SARS‐Cov‐2 invade the brain? Translational lessons from animal models

2020Journal article Open access
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dc.contributor.authorNatoli, S.
dc.contributor.authorOliveira, V.
dc.contributor.authorCalabresi, P.
dc.contributor.authorMaia, Luis
dc.contributor.authorPisani, A.
dc.date.accessioned2021-11-23T12:07:58Z
dc.date.available2021-11-23T12:07:58Z
dc.date.issued2020
dc.description.abstractThe current coronavirus disease (COVID-19) outbreak, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has raised the possibility of potential neurotropic properties of this virus. Indeed, neurological sequelae of SARS-CoV-2 infection have already been reported and highlight the relevance of considering the neurological impact of coronavirus (CoV) from a translational perspective. Animal models of SARS and Middle East respiratory syndrome, caused by structurally similar CoVs during the 2002 and 2012 epidemics, have provided valuable data on nervous system involvement by CoVs and the potential for central nervous system spread of SARS-CoV-2. One key finding that may unify these pathogens is that all require angiotensin-converting enzyme 2 as a cell entry receptor. The CoV spike glycoprotein, by which SARS-CoV-2 binds to cell membranes, binds angiotensin-converting enzyme 2 with a higher affinity compared with SARS-CoV. The expression of this receptor in neurons and endothelial cells hints that SARS-CoV-2 may have higher neuroinvasive potential compared with previous CoVs. However, it remains to be determined how such invasiveness might contribute to respiratory failure or cause direct neurological damage. Both direct and indirect mechanisms may be of relevance. Clinical heterogeneity potentially driven by differential host immune-mediated responses will require extensive investigation. Development of disease models to anticipate emerging neurological complications and to explore mechanisms of direct or immune-mediated pathogenicity in the short and medium term is therefore of great importance. In this brief review, we describe the current knowledge from models of previous CoV infections and discuss their potential relevance to COVID-19.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationNatoli S, Oliveira V, Calabresi P, Maia LF, Pisani A. Does SARS-Cov-2 invade the brain? Translational lessons from animal models. Eur J Neurol. 2020;27(9):1764-1773. doi:10.1111/ene.14277pt_PT
dc.identifier.doi10.1111/ene.14277pt_PT
dc.identifier.issn1351-5101
dc.identifier.issn1468-1331
dc.identifier.urihttp://hdl.handle.net/10400.16/2618
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.relation.publisherversionhttps://onlinelibrary.wiley.com/doi/10.1111/ene.14277pt_PT
dc.subjectCOVID-19pt_PT
dc.subjectSARS-CoV-2pt_PT
dc.subjectanimal modelspt_PT
dc.subjectcoronaviruspt_PT
dc.subjectneurotropismpt_PT
dc.subjectsystematic reviewpt_PT
dc.subjectviral infectionspt_PT
dc.titleDoes SARS‐Cov‐2 invade the brain? Translational lessons from animal modelspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceEnglandpt_PT
oaire.citation.endPage1773pt_PT
oaire.citation.issue9pt_PT
oaire.citation.startPage1764pt_PT
oaire.citation.titleEuropean Journal of Neurologypt_PT
oaire.citation.volume27pt_PT
person.familyNameMaia
person.givenNameLuis
person.identifier.ciencia-id9F1E-51AF-C38B
person.identifier.orcid0000-0002-8140-3471
person.identifier.ridJ-1742-2014
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication2b17a107-4559-498c-82f9-559a1ded4cac
relation.isAuthorOfPublication.latestForDiscovery2b17a107-4559-498c-82f9-559a1ded4cac

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