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dc.contributor.authorRende, Francescaen_US
dc.contributor.authorCavallari, Ilariaen_US
dc.contributor.authorAndresen, Vibekeen_US
dc.contributor.authorValeri, Valerio W.en_US
dc.contributor.authorD'Agostino, Donna M.en_US
dc.contributor.authorFranchini, Genoveffaen_US
dc.contributor.authorCiminale, Vincenzoen_US
dc.date.accessioned2016-02-24T14:19:09Z
dc.date.available2016-02-24T14:19:09Z
dc.date.issued2015-07-02
dc.PublishedRetrovirology 2015, 12:58eng
dc.identifier.issn1742-4690
dc.identifier.urihttps://hdl.handle.net/1956/11315
dc.description.abstractBackground: Human T cell leukemia virus type 1 (HTLV-1) gene expression is controlled by the key regulatory proteins Tax and Rex. The concerted action of these proteins results in a two-phase kinetics of viral expression that depends on a time delay between their action. However, it is difficult to explain this delay, as Tax and Rex are produced from the same mRNA. In the present study we investigated whether HTLV-1 may produce novel mRNA species capable of expressing Rex and Tax independently. Findings: Results revealed the expression of three alternatively spliced transcripts coding for novel Rex isoforms in infected cell lines and in primary samples from infected patients. One mRNA coded for a Tax isoform and a Rex isoform, and two mRNAs coded for Rex isoforms but not Tax. Functional assays showed that these Rex isoforms exhibit activity comparable to canonic Rex. An analysis of the temporal expression of these transcripts upon ex vivo culture of cells from infected patients and cell lines transfected with a molecular clone of HTLV-1 revealed early expression of the dicistronic tax/rex mRNAs followed by the monocistronic mRNAs coding for Rex isoforms. Conclusion: The production of monocistronic HTLV-1 mRNAs encoding Rex isoforms with comparable activity to canonical Rex, but with distinct timing, would support a prolonged duration of Rex function with gradual loss of Tax, and is consistent with the two-phase expression kinetics. A thorough understanding of these regulatory circuits will shed light on the basis of viral latency and provide groundwork to develop strategies for eradicating persistent infections.en_US
dc.language.isoengeng
dc.publisherBioMed Centraleng
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/4.0eng
dc.subjectHTLV-1eng
dc.subjectRexeng
dc.subjectSplicingeng
dc.titleIdentification of novel monocistronic HTLV-1 mRNAs encoding functional Rex isoformsen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2015-11-09T14:22:38Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2015 The Authors
dc.identifier.doihttps://doi.org/10.1186/s12977-015-0184-2
dc.identifier.cristin1262704
dc.subject.nsiVDP::Medisinske fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714
dc.subject.nsiVDP::Midical sciences: 700::Basic medical, dental and veterinary sciences: 710::Medical genetics: 714


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