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dc.contributor.authorWest, Caraen
dc.contributor.authorRus, Florentinaen
dc.contributor.authorChen, Yingen
dc.contributor.authorKleino, Annien
dc.contributor.authorGangloff, Moniqueen
dc.contributor.authorGammon, Don Ben
dc.contributor.authorSilverman, Nealen
dc.date.accessioned2019-05-03T23:32:32Z
dc.date.available2019-05-03T23:32:32Z
dc.date.issued2019-05en
dc.identifier.issn1999-4915
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/292410
dc.description.abstract<jats:p>The host immune response and virus-encoded immune evasion proteins pose constant, mutual selective pressure on each other. Virally encoded immune evasion proteins also indicate which host pathways must be inhibited to allow for viral replication. Here, we show that IIV-6 is capable of inhibiting the two Drosophila NF-κB signaling pathways, Imd and Toll. Antimicrobial peptide (AMP) gene induction downstream of either pathway is suppressed when cells infected with IIV-6 are also stimulated with Toll or Imd ligands. We find that cleavage of both Imd and Relish, as well as Relish nuclear translocation, three key points in Imd signal transduction, occur in IIV-6 infected cells, indicating that the mechanism of viral inhibition is farther downstream, at the level of Relish promoter binding or transcriptional activation. Additionally, flies co-infected with both IIV-6 and the Gram-negative bacterium, Erwinia carotovora carotovora, succumb to infection more rapidly than flies singly infected with either the virus or the bacterium. These findings demonstrate how pre-existing infections can have a dramatic and negative effect on secondary infections, and establish a Drosophila model to study confection susceptibility.</jats:p>
dc.format.mediumElectronicen
dc.languageengen
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAnimalsen
dc.subjectDrosophila melanogasteren
dc.subjectIridovirusen
dc.subjectDrosophila Proteinsen
dc.subjectTranscription Factorsen
dc.subjectVirus Replicationen
dc.subjectToll-Like Receptorsen
dc.subjectHost-Pathogen Interactionsen
dc.subjectImmunity, Innateen
dc.titleIIV-6 Inhibits NF-κB Responses in <i>Drosophila</i>.en
dc.typeArticle
prism.issueIdentifier5en
prism.publicationDate2019en
prism.publicationNameVirusesen
prism.volume11en
dc.identifier.doi10.17863/CAM.39560
dcterms.dateAccepted2019-04-28en
rioxxterms.versionofrecord10.3390/v11050409en
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-05en
dc.contributor.orcidKleino, Anni [0000-0001-8919-9404]
dc.contributor.orcidGangloff, Monique [0000-0001-6131-0115]
dc.contributor.orcidSilverman, Neal [0000-0002-4259-456X]
dc.identifier.eissn1999-4915
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idWellcome Trust (100321/Z/12/Z)
pubs.funder-project-idMRC (MR/P02260X/1)


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International