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dc.contributor.authorLopez-Huertas, Maria Rosa 
dc.contributor.authorJiménez-Tormo, Laura
dc.contributor.authorMadrid-Elena, Nadia
dc.contributor.authorGutiérrez, Carolina
dc.contributor.authorRodríguez-Mora, Sara 
dc.contributor.authorCoiras, Mayte 
dc.contributor.authorAlcamí, José 
dc.contributor.authorMoreno, Santiago
dc.date.accessioned2019-03-14T12:00:31Z
dc.date.available2019-03-14T12:00:31Z
dc.date.issued2017-03
dc.identifier.citationSci Rep. 2017 May;7(1):2385.es_ES
dc.identifier.issn2045-2322es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7333
dc.description.abstractA potential strategy to cure HIV-1 infection is to use latency reversing agents (LRAs) to eliminate latent reservoirs established in resting CD4+ T (rCD4+) cells. As no drug has been shown to be completely effective, finding new drugs and combinations are of increasing importance. We studied the effect of Maraviroc (MVC), a CCR5 antagonist that activates NF-κB, on HIV-1 replication from latency. HIV-1-latency models based on CCL19 or IL7 treatment, before HIV-1 infection were used. Latently infected primary rCD4+ or central memory T cells were stimulated with MVC alone or in combination with Bryostatin-1, a PKC agonist known to reverse HIV-1 latency. MVC 5 μM and 0.31 μM were chosen for further studies although other concentrations of MVC also increased HIV-1 replication. MVC was as efficient as Bryostatin-1 in reactivating X4 and R5-tropic HIV-1. However, the combination of MVC and Bryostatin-1 was antagonistic, probably because Bryostatin-1 reduced CCR5 expression levels. Although HIV-1 reactivation had the same tendency in both latency models, statistical significance was only achieved in IL7-treated cells. These data suggest that MVC should be regarded as a new LRA with potency similar as Bryostatin-1. Further studies are required to describe the synergistic effect of MVC with other LRAs.es_ES
dc.description.sponsorshipThe authors would like to acknowledge the staff at the Institute of Health Carlos III (National Centre for Microbiology, Madrid, Spain) for their support.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Group es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectMaraviroces_ES
dc.subjectBryostatines_ES
dc.subjectHIV latencyes_ES
dc.subjectHIV cure
dc.subjectLRA
dc.subject.meshBryostatins es_ES
dc.subject.meshCCR5 Receptor Antagonists es_ES
dc.subject.meshCD4-Positive T-Lymphocytes es_ES
dc.subject.meshCell Proliferation es_ES
dc.subject.meshChemokine CCL19 es_ES
dc.subject.meshGene Expression Regulation es_ES
dc.subject.meshHIV-1 es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInterleukin-7 es_ES
dc.subject.meshMaraviroc es_ES
dc.subject.meshNF-kappa B es_ES
dc.subject.meshPrimary Cell Culture es_ES
dc.subject.meshProtein Kinase C es_ES
dc.subject.meshReceptors, CCR5 es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshVirus Latency es_ES
dc.subject.meshVirus Replication es_ES
dc.subject.meshHost-Pathogen Interactions es_ES
dc.titleThe CCR5-antagonist Maraviroc reverses HIV-1 latency in vitro alone or in combination with the PKC-agonist Bryostatin-1es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID28539614es_ES
dc.format.volume7es_ES
dc.format.number1es_ES
dc.format.page2385es_ES
dc.identifier.doi10.1038/s41598-017-02634-yes_ES
dc.description.peerreviewedNoes_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41598-017-02634-yes_ES
dc.identifier.journalScientific reportses_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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