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dc.contributor.authorFitzsimmons, L
dc.contributor.authorKelly, GL
dc.date.accessioned2020-12-21T04:04:24Z
dc.date.available2020-12-21T04:04:24Z
dc.date.issued2017-11-01
dc.identifierpii: v9110339
dc.identifier.citationFitzsimmons, L. & Kelly, G. L. (2017). EBV and Apoptosis: The Viral Master Regulator of Cell Fate?. VIRUSES-BASEL, 9 (11), https://doi.org/10.3390/v9110339.
dc.identifier.issn1999-4915
dc.identifier.urihttp://hdl.handle.net/11343/257471
dc.description.abstractEpstein-Barr virus (EBV) was first discovered in cells from a patient with Burkitt lymphoma (BL), and is now known to be a contributory factor in 1-2% of all cancers, for which there are as yet, no EBV-targeted therapies available. Like other herpesviruses, EBV adopts a persistent latent infection in vivo and only rarely reactivates into replicative lytic cycle. Although latency is associated with restricted patterns of gene expression, genes are never expressed in isolation; always in groups. Here, we discuss (1) the ways in which the latent genes of EBV are known to modulate cell death, (2) how these mechanisms relate to growth transformation and lymphomagenesis, and (3) how EBV genes cooperate to coordinately regulate key cell death pathways in BL and lymphoblastoid cell lines (LCLs). Since manipulation of the cell death machinery is critical in EBV pathogenesis, understanding the mechanisms that underpin EBV regulation of apoptosis therefore provides opportunities for novel therapeutic interventions.
dc.languageEnglish
dc.publisherMDPI AG
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleEBV and Apoptosis: The Viral Master Regulator of Cell Fate?
dc.typeJournal Article
dc.identifier.doi10.3390/v9110339
melbourne.affiliation.departmentMedical Biology (W.E.H.I.)
melbourne.source.titleViruses
melbourne.source.volume9
melbourne.source.issue11
dc.rights.licenseCC BY
melbourne.elementsid1275492
melbourne.contributor.authorKelly, Gemma
dc.identifier.eissn1999-4915
melbourne.accessrightsOpen Access


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