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      <subfield code="a">Lopez-Huertas, Maria Rosa</subfield>
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      <subfield code="a">Jiménez-Tormo, Laura</subfield>
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      <subfield code="a">Madrid-Elena, Nadia</subfield>
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      <subfield code="a">Gutiérrez, Carolina</subfield>
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      <subfield code="a">Rodríguez-Mora, Sara</subfield>
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      <subfield code="a">Coiras, Mayte</subfield>
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      <subfield code="a">Moreno, Santiago</subfield>
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      <subfield code="a">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.</subfield>
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      <subfield code="a">Sci Rep. 2017 May;7(1):2385.</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/7333</subfield>
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      <subfield code="a">The CCR5-antagonist Maraviroc reverses HIV-1 latency in vitro alone or in combination with the PKC-agonist Bryostatin-1</subfield>
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