Lopez-Huertas, Maria RosaJiménez-Tormo, LauraMadrid-Elena, NadiaGutiérrez, CarolinaRodríguez-Mora, SaraCoiras, MayteAlcamí, JoséMoreno, Santiago2019-03-142019-03-142017-03Sci Rep. 2017 May;7(1):2385.2045-2322http://hdl.handle.net/20.500.12105/7333A 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.engVoRhttp://creativecommons.org/licenses/by-nc-sa/4.0/MaravirocBryostatinHIV latencyHIV cureLRABryostatinsCCR5 Receptor AntagonistsCD4-Positive T-LymphocytesCell ProliferationChemokine CCL19Gene Expression RegulationHIV-1HumansInterleukin-7MaravirocNF-kappa BPrimary Cell CultureProtein Kinase CReceptors, CCR5Signal TransductionVirus LatencyVirus ReplicationHost-Pathogen InteractionsAtribución-NoComercial-CompartirIgual 4.0 Internacional2853961471238510.1038/s41598-017-02634-yScientific reportsopen access