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- W2955711170 abstract "HIV-1 Tat enhances viral RNA transcription by binding to TAR and recruiting activating factors. Tat enhances its own transcription via a positive-feedback loop. Didehydro-cortistatin A (dCA) is a potent Tat inhibitor, reducing HIV-1 transcription and preventing viral rebound. dCA activity demonstrates the potential of the “block-and-lock” functional cure approaches. We investigated the viral genetic barrier to dCA resistance in vitro . While mutations in Tat and TAR were not identified, mutations in the promoter and in the Nef and Vpr proteins promoted high Tat-independent activity. Promoter mutations increased the basal transcription, while Nef and Vpr mutations increased NF-κB nuclear translocation. This heightened transcriptional activity renders CD4 + T cells infected with these viruses more susceptible to cytotoxic T cell-mediated killing and to cell death by cytopathic effects. Results provide insights on drug resistance to a novel class of antiretrovirals and reveal novel aspects of viral transcriptional regulation." @default.
- W2955711170 created "2019-07-12" @default.
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- W2955711170 date "2019-08-27" @default.
- W2955711170 modified "2023-10-16" @default.
- W2955711170 title "Resistance to the Tat Inhibitor Didehydro-Cortistatin A Is Mediated by Heightened Basal HIV-1 Transcription" @default.
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- W2955711170 doi "https://doi.org/10.1128/mbio.01750-18" @default.
- W2955711170 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6606815" @default.
- W2955711170 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31266880" @default.
- W2955711170 hasPublicationYear "2019" @default.
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