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dc.contributor.author | Lopez-Huertas, Maria Rosa | |
dc.contributor.author | Jiménez-Tormo, Laura | |
dc.contributor.author | Madrid-Elena, Nadia | |
dc.contributor.author | Gutiérrez, Carolina | |
dc.contributor.author | Rodríguez-Mora, Sara | |
dc.contributor.author | Coiras, Mayte | |
dc.contributor.author | Alcamí, José | |
dc.contributor.author | Moreno, Santiago | |
dc.date.accessioned | 2019-03-14T12:00:31Z | |
dc.date.available | 2019-03-14T12:00:31Z | |
dc.date.issued | 2017-03 | |
dc.identifier.citation | Sci Rep. 2017 May;7(1):2385. | es_ES |
dc.identifier.issn | 2045-2322 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/7333 | |
dc.description.abstract | A 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.sponsorship | The 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.iso | eng | es_ES |
dc.publisher | Nature Publishing Group | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.subject | Maraviroc | es_ES |
dc.subject | Bryostatin | es_ES |
dc.subject | HIV latency | es_ES |
dc.subject | HIV cure | |
dc.subject | LRA | |
dc.subject.mesh | Bryostatins | es_ES |
dc.subject.mesh | CCR5 Receptor Antagonists | es_ES |
dc.subject.mesh | CD4-Positive T-Lymphocytes | es_ES |
dc.subject.mesh | Cell Proliferation | es_ES |
dc.subject.mesh | Chemokine CCL19 | es_ES |
dc.subject.mesh | Gene Expression Regulation | es_ES |
dc.subject.mesh | HIV-1 | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Interleukin-7 | es_ES |
dc.subject.mesh | Maraviroc | es_ES |
dc.subject.mesh | NF-kappa B | es_ES |
dc.subject.mesh | Primary Cell Culture | es_ES |
dc.subject.mesh | Protein Kinase C | es_ES |
dc.subject.mesh | Receptors, CCR5 | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Virus Latency | es_ES |
dc.subject.mesh | Virus Replication | es_ES |
dc.subject.mesh | Host-Pathogen Interactions | es_ES |
dc.title | The CCR5-antagonist Maraviroc reverses HIV-1 latency in vitro alone or in combination with the PKC-agonist Bryostatin-1 | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución-NoComercial-CompartirIgual 4.0 Internacional | * |
dc.identifier.pubmedID | 28539614 | es_ES |
dc.format.volume | 7 | es_ES |
dc.format.number | 1 | es_ES |
dc.format.page | 2385 | es_ES |
dc.identifier.doi | 10.1038/s41598-017-02634-y | es_ES |
dc.description.peerreviewed | No | es_ES |
dc.relation.publisherversion | https://doi.org/10.1038/s41598-017-02634-y | es_ES |
dc.identifier.journal | Scientific reports | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.rights.accessRights | open access | es_ES |