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dc.contributor.authorMaillard, PV
dc.contributor.authorVeen, AG
dc.contributor.authorPoirier, EZ
dc.contributor.authorReis e Sousa, C
dc.date.accessioned2020-06-08T17:00:10Z
dc.date.available2019-01-25
dc.date.available2020-06-08T17:00:10Z
dc.date.issued2019-04-15
dc.identifier.issn0261-4189
dc.identifier.urihttps://qmro.qmul.ac.uk/xmlui/handle/123456789/64720
dc.description.abstractTo protect against the harmful consequences of viral infections, organisms are equipped with sophisticated antiviral mechanisms, including cell‐intrinsic means to restrict viral replication and propagation. Plant and invertebrate cells utilise mostly RNA interference (RNA i), an RNA ‐based mechanism, for cell‐intrinsic immunity to viruses while vertebrates rely on the protein‐based interferon (IFN )‐driven innate immune system for the same purpose. The RNA i machinery is conserved in vertebrate cells, yet whether antiviral RNA i is still active in mammals and functionally relevant to mammalian antiviral defence is intensely debated. Here, we discuss cellular and viral factors that impact on antiviral RNA i and the contexts in which this system might be at play in mammalian resistance to viral infection.en_US
dc.languageen
dc.language.isoenen_US
dc.publisherEMBOen_US
dc.relation.ispartofThe EMBO Journal
dc.rightsCreative Commons Attribution 4.0 License
dc.titleSlicing and dicing viruses: antiviral RNA interference in mammalsen_US
dc.typeArticleen_US
dc.identifier.doi10.15252/embj.2018100941
pubs.issue8en_US
pubs.notesNot knownen_US
pubs.publication-statusPublisheden_US
pubs.volume38en_US
dcterms.dateAccepted2019-01-25
rioxxterms.funderDefault funderen_US
rioxxterms.identifier.projectDefault projecten_US


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