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Chromatin reassembly factors are involved in transcriptional interference promoting HIV latency

 

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dc.creator Gallastegui, Edurne es
dc.creator Millán Zambrano, Gonzalo es
dc.creator Terme, Jean Michel es
dc.creator Chávez de Diego, Sebastián es
dc.creator Jordan, Albert es
dc.date.accessioned 2017-08-01T15:52:17Z
dc.date.available 2017-08-01T15:52:17Z
dc.date.issued 2011-04
dc.identifier.citation Gallastegui, E., Millán Zambrano, G., Terme, J.M., Chávez de Diego, S. y Jordan, A. (2011). Chromatin reassembly factors are involved in transcriptional interference promoting HIV latency. Journal of Virology, 85 (7), 3187-3202.
dc.identifier.issn 0022-538X (impreso) es
dc.identifier.issn 1098-5514 (electronico) es
dc.identifier.uri http://hdl.handle.net/11441/63474
dc.description.abstract The establishment of a stable reservoir of latently infected cells allows HIV to persist in the host. Usually, HIV infection of T cells results in integration of the viral genome, with a preference for regions in the human genome containing active genes, viral expression, and production of new viruses. However, in rare cases T cells become latently infected, and this is presumed to be due to a combination of two factors: integrated viruses are not efficiently transcribed and infected T cells revert to a resting memory state. HIV latency has been associated with provirus integration in regions of constitutive heterochromatin, gene deserts, or very highly expressed genes. We have investigated the transcriptional consequences of latent HIV integration into cellular genes and the involvement of chromatin reassembly factors (CRFs) in the transcriptional interference that a host gene exerts on the integrated cryptic HIV promoter. Chimeric transcripts containing sequences from the host gene and HIV can be detected, having been initiated at promoters of either the cell or the virus. Reactivation of HIV downregulates host gene expression. Cryptic promoters might remain inactive due to the repressive chromatin configuration established by CRFs during transcription elongation. Depletion of CRFs such as Spt6, Chd1, and FACT, or the histone chaperones ASF1a and HIRA, promoted HIV reactivation, concomitantly with chromatin relaxation and a decrease in general RNA polymerase activity. Overall, our results indicate that CRFs play a role in maintaining HIV latency by transcriptional interference when the provirus is integrated into an intron of a highly active gene. es
dc.description.sponsorship Fundación para la Investigación y Prevención del SIDA FIPSE, 36602/06 es
dc.description.sponsorship Ministerio de Ciencia e Innovación y FEDER BFU2008-00359/BMC es
dc.description.sponsorship Ministerio de Economía, Industria y Competitividad BFU2007-67575-C03-02/BMC es
dc.description.sponsorship Gobierno de Andalucía P07-CVI-02623 es
dc.format application/pdf es
dc.language.iso eng es
dc.publisher American Society for Microbiology es
dc.relation.ispartof Journal of Virology, 85 (7), 3187-3202.
dc.rights Attribution-NonCommercial-NoDerivatives 4.0 Internacional *
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/ *
dc.title Chromatin reassembly factors are involved in transcriptional interference promoting HIV latency es
dc.type info:eu-repo/semantics/article es
dc.type.version info:eu-repo/semantics/publishedVersion es
dc.rights.accessrights info:eu-repo/semantics/openAccess es
dc.contributor.affiliation Universidad de Sevilla. Departamento de Genética es
dc.relation.projectID FIPSE, 36602/06 es
dc.relation.projectID BFU2008-00359/BMC es
dc.relation.projectID info:eu-repo/grantAgreement/MINECO/BFU2007-67575-C03-02/BMC es
dc.relation.projectID P07-CVI-02623 es
dc.relation.publisherversion http://dx.doi.org/10.1128/JVI.01920-10 es
dc.identifier.doi 10.1128/JVI.01920-10 es
idus.format.extent 16 p. es
dc.journaltitle Journal of Virology es
dc.publication.volumen 85 es
dc.publication.issue 7 es
dc.publication.initialPage 3187 es
dc.publication.endPage 3202 es
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