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- W2006364509 abstract "Despite its clinical importance, the molecular biology of HIV-1 latency control is at best partially understood, and the literature remains conflicting. The most recent description that latent HIV-1 is integrated into actively expressed host genes has further confounded the situation. This lack of molecular understanding complicates our efforts to identify therapeutic compounds or strategies that could reactivate latent HIV-1 infection in patients, a prerequisite for the eradication of HIV-1 infection. Currently, many therapeutic development efforts operate under the assumption that a restrictive histone code could govern latent infection and that either dissipation of the histone-based restrictions or NF-κB activation could be sufficient to trigger HIV-1 reactivation. We here present data that suggest an additional, higher level of molecular control. During a high-content drug screening effort, we identified AS601245 as a potent inhibitor of HIV-1 reactivation in latently infected primary T cells and T cell lines. In either system, AS601245 inhibited HIV-1 reactivation despite high levels of induced NF-κB activation. This finding suggests the presence of a gatekeeper kinase activity that controls latent HIV-1 infection even in the presence of high levels of NF-κB activity. Potential therapeutic stimuli that do not target this gatekeeper kinase will likely fail to trigger efficient system-wide HIV-1 reactivation." @default.
- W2006364509 created "2016-06-24" @default.
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- W2006364509 date "2012-04-15" @default.
- W2006364509 modified "2023-10-16" @default.
- W2006364509 title "Kinase Control Prevents HIV-1 Reactivation in Spite of High Levels of Induced NF-κB Activity" @default.
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- W2006364509 doi "https://doi.org/10.1128/jvi.06726-11" @default.
- W2006364509 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3318643" @default.
- W2006364509 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22345467" @default.
- W2006364509 hasPublicationYear "2012" @default.
- W2006364509 type Work @default.