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dc.rights.licenseopenen_US
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorDAMOUR, Alexia
hal.structure.identifierInstitut de génétique humaine [IGH]
dc.contributor.authorSLANINOVA, Vera
hal.structure.identifierLaboratory of Pathogen and Host Immunity [Montpellier] [LPHI]
dc.contributor.authorRADULESCU, Ovidiu
hal.structure.identifierInstitut de génétique humaine [IGH]
dc.contributor.authorBERTRAND, Edouard
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorBASYUK, Eugenia
dc.date.accessioned2024-04-24T10:50:29Z
dc.date.available2024-04-24T10:50:29Z
dc.date.issued2023-09
dc.identifier.issn1999-4915en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/199311
dc.description.abstractEnThis review summarizes current advances in the role of transcriptional stochasticity in HIV-1 latency, which were possible in a large part due to the development of single-cell approaches. HIV-1 transcription proceeds in bursts of RNA production, which stem from the stochastic switching of the viral promoter between ON and OFF states. This switching is caused by random binding dynamics of transcription factors and nucleosomes to the viral promoter and occurs at several time scales from minutes to hours. Transcriptional bursts are mainly controlled by the core transcription factors TBP, SP1 and NF-κb, the chromatin status of the viral promoter and RNA polymerase II pausing. In particular, spontaneous variability in the promoter chromatin creates heterogeneity in the response to activators such as TNF-α, which is then amplified by the Tat feedback loop to generate high and low viral transcriptional states. This phenomenon is likely at the basis of the partial and stochastic response of latent T cells from HIV-1 patients to latency-reversing agents, which is a barrier for the development of shock-and-kill strategies of viral eradication. A detailed understanding of the transcriptional stochasticity of HIV-1 and the possibility to precisely model this phenomenon will be important assets to develop more effective therapeutic strategies.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enHIV-1 latency; transcription; transcriptional noise; transcriptional burst; promoter; transcription factor; chromatin; integration site; modeling
dc.title.enTranscriptional Stochasticity as a Key Aspect of HIV-1 Latency
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/v15091969en_US
dc.subject.halSciences du Vivant [q-bio]en_US
dc.identifier.pubmed37766375en_US
bordeaux.journalVirusesen_US
bordeaux.page1969en_US
bordeaux.volume15en_US
bordeaux.hal.laboratoriesMFP (Laboratoire Microbiologie Fondamentale et Pathogénicité) - UMR 5234en_US
bordeaux.issue9en_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcehal
hal.identifierhal-04235056
hal.version1
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
workflow.import.sourcehal
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Viruses&rft.date=2023-09&rft.volume=15&rft.issue=9&rft.spage=1969&rft.epage=1969&rft.eissn=1999-4915&rft.issn=1999-4915&rft.au=DAMOUR,%20Alexia&SLANINOVA,%20Vera&RADULESCU,%20Ovidiu&BERTRAND,%20Edouard&BASYUK,%20Eugenia&rft.genre=article


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