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HIV-1 nucleocapsid and ESCRT-component Tsg101 interplay prevents HIV from turning into a DNA-containing virus

dc.contributor.authorCHAMONTIN, Célia
dc.contributor.authorRASSAM, Patrice
dc.contributor.authorFERRER, Mireia
dc.contributor.authorRACINE, Pierre-Jean
dc.contributor.authorNEYRET, Aymeric
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorLAINÉ, Sébastien
dc.contributor.authorMILHIET, Pierre-Emmanuel
dc.contributor.authorMOUGEL, Marylène
dc.date.accessioned2023-07-18T08:34:16Z
dc.date.available2023-07-18T08:34:16Z
dc.date.issued2015
dc.identifier.issn0305-1048
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/183423
dc.description.abstractEnHIV-1, the agent of the AIDS pandemic, is an RNA virus that reverse transcribes its RNA genome (gRNA) into DNA, shortly after its entry into cells. Within cells, retroviral assembly requires thousands of structural Gag proteins and two copies of gRNA as well as cellular factors, which converge to the plasma membrane in a finely regulated timeline. In this process, the nucleocapsid domain of Gag (GagNC) ensures gRNA selection and packaging into virions. Subsequent budding and virus release require the recruitment of the cellular ESCRT machinery. Interestingly, mutating GagNC results into the release of DNA-containing viruses, by promoting reverse transcription (RTion) prior to virus release , through an unknown mechanism. Therefore, we explored the biogenesis of these DNA-containing particles, combining live-cell total internal-reflection fluorescent microscopy, electron microscopy, trans-complementation assays and biochemical characterization of viral particles. Our results reveal that DNA virus production is the consequence of budding defects associated with Gag aggregation at the plasma membrane and deficiency in the recruitment of Tsg101, a key ESCRT-I component. Indeed, targeting Tsg101 to virus assembly sites restores budding , restricts RTion and favors RNA packaging into viruses. Altogether, our results highlight the role of GagNC in the spatiotemporal control of RTion, via an ESCRT-I-dependent mechanism.
dc.language.isoen
dc.publisherOxford University Press
dc.rights.urihttp://creativecommons.org/licenses/by-nc/
dc.title.enHIV-1 nucleocapsid and ESCRT-component Tsg101 interplay prevents HIV from turning into a DNA-containing virus
dc.typeArticle de revueen_US
dc.identifier.doi10.1093/nar/gku1232
dc.subject.halSciences du Vivant [q-bio]/Microbiologie et Parasitologie/Virologie
dc.subject.halSciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire/Génomique, Transcriptomique et Protéomique [q-bio.GN]
bordeaux.page336-347
bordeaux.volume43
bordeaux.hal.laboratoriesMFP (Laboratoire Microbiologie Fondamentale et Pathogénicité) - UMR 5234en_US
bordeaux.issue1
bordeaux.institutionCNRS
bordeaux.peerReviewedoui
bordeaux.import.sourcehal
hal.identifierhal-01923835
hal.version1
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
workflow.import.sourcehal
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