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dc.contributor.advisorBowie, Andrew
dc.contributor.authorMulhern, Orla
dc.date.accessioned2019-11-13T11:58:59Z
dc.date.available2019-11-13T11:58:59Z
dc.date.issued2010
dc.identifier.citationOrla Mulhern, 'Modulation of innate immunity by the vaccinia virus protein K7 and its target DDX3', [thesis], Trinity College (Dublin, Ireland). School of Biochemistry and Immunology, 2010, pp 272
dc.identifier.otherTHESIS 9456
dc.identifier.urihttp://hdl.handle.net/2262/90424
dc.description.abstractVaccinia virus (VACV) has many mechanisms to subvert and modulate the host immune response. One well characterised VACV protein that does this is A52. K7 was found from a search of the VACV genome looking for genes with sequence similarities to A52. A52 is known to modulate IL-1 and TLR signalling and contributes to virulence. Like A52, K7 can inhibit interleukin-1 (IL-1) and toll-like receptor (TLR) signalling leading to NFkB aetivation. In addition both K7 and A52 can induce IL-10, an anti-inflammatory cytokine, to modulate the host response to VACV.
dc.format1 volume
dc.language.isoen
dc.publisherTrinity College (Dublin, Ireland). School of Biochemistry and Immunology
dc.relation.isversionofhttp://stella.catalogue.tcd.ie/iii/encore/record/C__Rb14882909
dc.subjectBiochemistry, Ph.D.
dc.subjectPh.D. Trinity College Dublin.
dc.titleModulation of innate immunity by the vaccinia virus protein K7 and its target DDX3
dc.typethesis
dc.type.supercollectionthesis_dissertations
dc.type.supercollectionrefereed_publications
dc.type.qualificationlevelDoctoral
dc.type.qualificationnameDoctor of Philosophy (Ph.D.)
dc.rights.ecaccessrightsopenAccess
dc.format.extentpaginationpp 272
dc.description.noteTARA (Trinity’s Access to Research Archive) has a robust takedown policy. Please contact us if you have any concerns: rssadmin@tcd.ie


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