HTLV-1 Tax activates HIV-1 transcription in latency models

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dc.creatorVictor Emmanuel Viana Geddes
dc.creatorDiego Pandeló José
dc.creatorFabio E. Leal
dc.creatorDouglas F. Nixon
dc.creatorAmilcar Tanuri
dc.creatorRenato Santana de Aguiar
dc.date.accessioned2023-07-14T22:49:43Z
dc.date.accessioned2025-09-08T23:27:52Z
dc.date.available2023-07-14T22:49:43Z
dc.date.issued2017
dc.identifier.doihttps://doi.org/10.1016/j.virol.2017.01.014
dc.identifier.issn0042-6822
dc.identifier.urihttps://hdl.handle.net/1843/56337
dc.languagepor
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofVirology
dc.rightsAcesso Aberto
dc.subjectHIV (Virus)
dc.subjectHTLV-I (Virus)
dc.subject.otherHIV-1
dc.subject.otherLatency
dc.subject.otherHTLV-1
dc.subject.otherTax
dc.subject.otherTax
dc.subject.otherResting cells
dc.titleHTLV-1 Tax activates HIV-1 transcription in latency models
dc.typeArtigo de periódico
local.citation.epage51
local.citation.spage45
local.citation.volume504
local.description.resumoHIV-1 latency is a major obstacle to HIV-1 eradication. Coinfection with HTLV-1 has been associated with faster progression to AIDS. HTLV-1 encodes the transactivator Tax which can activate both HTLV-1 and HIV-1 transcription. Here, we demonstrate that Tax activates HIV transcription in latent CD4+ T cells. Tax promotes the activation of P-TEFb, releasing CDK9 and Cyclin T1 from inactive forms, promoting transcription elongation and reactivation of latent HIV-1. Tax mutants lacking interaction with the HIV-1-LTR promoter were not able to activate P-TEFb, with no subsequent activation of latent HIV. In HIV-infected primary resting CD4+ T cells, Tax-1 reactivated HIV-1 transcription up to five fold, confirming these findings in an ex vivo latency model. Finally, our results confirms that HTLV-1/Tax hijacks cellular partners, promoting HIV-1 transcription, and this interaction should be further investigated in HIV-1 latency studies in patients with HIV/ HTLV-1 co-infection.
local.identifier.orcidhttps://orcid.org/0000-0002-0723-3873
local.identifier.orcidhttps://orcid.org/0000-0002-3243-5688
local.identifier.orcidhttps://orcid.org/0000-0002-2801-1786
local.identifier.orcidhttps://orcid.org/0000-0003-0570-750X
local.publisher.countryBrasil
local.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICAS
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/pii/S0042682217300235?via%3Dihub

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