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dc.creatorDuncan, Christopher J.A.
dc.creatorRandall, Richard E.
dc.creatorHambleton, Sophie
dc.date.accessioned2020-09-25T20:38:12Z
dc.date.available2020-09-25T20:38:12Z
dc.date.created2020
dc.identifier.issn1362-4555spa
dc.identifier.otherhttps://doi.org/10.1016/j.tig.2020.08.017spa
dc.identifier.urihttp://hdl.handle.net/20.500.12010/13831
dc.description.abstractThe concept that type I interferons (IFN-I) are essential to antiviral immunity derives from studies on animal models and cell lines. Virtually all pathogenic viruses have evolved countermeasures to IFN-I restriction, and genetic loss of viral IFN-I antagonists leads to virus attenuation. But just how important is IFN-I to antiviral defence in humans? The recent discovery of genetic defects of IFN-I signalling illuminates this and other questions of IFN biology, including the role of the mucosa-restricted type III IFNs (IFN-III), informing our understanding of the place of the IFN system within the concerted antiviral response. Here we review monogenic lesions of IFN-I signalling pathways and summarise the organising principles which emerge.spa
dc.format.extent13 páginasspa
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.publisherTrends in geneticsspa
dc.sourcereponame:Expeditio Repositorio Institucional UJTLspa
dc.sourceinstname:Universidad de Bogotá Jorge Tadeo Lozanospa
dc.subjectHuman antiviral immunityspa
dc.subjectGenetic lesionsspa
dc.titleGenetic lesions of type i interferon signalling in human antiviral immunityspa
dc.type.localArtículospa
dc.subject.lembSíndrome respiratorio agudo gravespa
dc.subject.lembCOVID-19spa
dc.subject.lembSARS-CoV-2spa
dc.subject.lembCoronavirusspa
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.type.hasversioninfo:eu-repo/semantics/acceptedVersionspa
dc.rights.localAbierto (Texto Completo)spa
dc.identifier.doihttps://doi.org/10.1016/j.tig.2020.08.017spa
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1spa


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