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dc.contributor.authorJose, Diego Pandelo
dc.contributor.authorBartholomeeusen, Koen
dc.contributor.authorda Cunha, Rodrigo Delvecchio
dc.contributor.authorAbreu, Celina Monteiro
dc.contributor.authorGlinski, Jan
dc.contributor.authorFerreira da Costa, Thais Barbizan
dc.contributor.authorMello Bacchi Rabay, Ana Flavia
dc.contributor.authorPianowski Filho, Luiz Francisco
dc.contributor.authorDudycz, Lech W.
dc.contributor.authorRanga, Udaykumar
dc.contributor.authorPeterlin, Boris Matija
dc.contributor.authorPianowski, Luiz Francisco
dc.contributor.authorTanuri, Amilcar
dc.contributor.authorAguiar, Renato Santana
dc.date.accessioned2017-02-21T08:55:13Z-
dc.date.available2017-02-21T08:55:13Z-
dc.date.issued2014
dc.identifier.citationJose, DP; Bartholomeeusen, K; da Cunha, RD; Abreu, CM; Glinski, J; da Costa, TBF; Rabay, AFMB; Pianowski, LF; Dudycz, LW; Ranga, U; Peterlin, BM; Pianowski, LF; Tanuri, A; Aguiar, RS, Reactivation of latent HIV-1 by new semi-synthetic ingenol esters. Virology 2014, 462, 328-339, http://dx.doi.org/10.1016/j.virol.2014.05.033en_US
dc.identifier.citationVirologyen_US
dc.identifier.citation462en_US
dc.identifier.issn0042-6822
dc.identifier.urihttp://hdl.handle.net/10572/2481-
dc.descriptionRestricted Accessen_US
dc.description.abstractThe ability of HIV to establish long-lived latent infection is mainly due to transcriptional silencing of viral genome in resting memory T lymphocytes. Here, we show that new semi-synthetic ingenol esters reactivate latent HIV reservoirs. Amongst the tested compounds, 3-caproyl-ingenol (ING B) was more potent in reactivating latent HIV than known activators such as SAHA, ingenol 3,20-dibenzoate, TNF-alpha, PMA and HMBA. ING B activated PKC isoforms followed by NF-kappa B nuclear translocation. As virus reactivation is dependent on intact NF-kappa B binding sites in the LTR promoter region ING B, we have shown that. ING B was able to reactivate virus transcription in primary HIV-infected resting cells up to 12 fold and up to 25 fold in combination with SAHA. Additionally, ING B promoted up-regulation of P-TEFb subunits CDK9/Cyclin TI. The role of ING B on promoting both transcription initiation and elongation makes this compound a strong candidate for an anti-HIV latency drug combined with suppressive HAART. (C) 2014 Elsevier Inc. All rights reserved.en_US
dc.description.urihttp://dx.doi.org/10.1016/j.virol.2014.05.033en_US
dc.language.isoEnglishen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.rights@Academic Press Inc Elsevier Science, 2014en_US
dc.subjectVirologyen_US
dc.subjectHIVen_US
dc.subjectLatencyen_US
dc.subjectIngenolen_US
dc.subjectPkcen_US
dc.subjectNf-Kappa Ben_US
dc.subjectResting Cellsen_US
dc.subjectP-Tefben_US
dc.subjectNf-Kappa-Ben_US
dc.subjectProtein-Kinase-Cen_US
dc.subjectImmunodeficiency-Virus Type-1en_US
dc.subjectSuberoylanilide Hydroxamic Aciden_US
dc.subjectActive Antiretroviral Therapyen_US
dc.subjectT-Lymphocytesen_US
dc.subjectP-Tefben_US
dc.subjectSubtype Cen_US
dc.subjectDeacetylase Inhibitorsen_US
dc.subjectGene-Expressionen_US
dc.titleReactivation of latent HIV-1 by new semi-synthetic ingenol estersen_US
dc.typeArticleen_US
Appears in Collections:Research Papers (Ravi Manjithaya)

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