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Human immunodeficiency virus 1 strain:Subtype B

ABSTRACT: Utilization of HIV-1 envelope V3 to identify X4- and R5-specific Tat and LTR sequence signatures

PROVIDER: PRJNA319822 | ENA |

REPOSITORIES: ENA

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Identification of HIV Tat and NF-kB binding proteins associated with semen derived extracellular vesicles. In this study, we used orthogonal pull-downs, mobility shift, and electrophoretic protein binding assays coupled with proteomic and secretomic analyses to highlights the previously unappreciated SEV-associated transcriptional repressors that may target HIV Tat to suppress viral transcription.

Project description:Semen-derived extracellular vesicles (SEVs) have been shown to inhibit the human immunodeficiency virus type 1 (HIV-1) LTR transactivation through the blockade of the interaction of transactivator of transcription (Tat) and host transcription factors NF-kB and Sp1 (Tat•NF-ᴋB p65 and Tat•Sp1). The ability of SEVs to regulate the activities of transcription factors suggests that SEVs may contain transcription activators and repressors. In this present study, we used orthogonal SEVs-based screens, including pull-downs, mobility shift assays, and electrophoretic protein binding assays coupled with mass spectrometry (MS) to identify host proteins in SEVs that interact with the different transcription factors (SEVs•Tat and SEVs•NF-ᴋB p65 binding proteins). Protein network analysis performed on SEVs•Tat and SEVs•NF-ᴋB p65 complexes revealed interactome networks that associate with 7SK snRNA binding, mRNA Processing, P-TEFb complex, NELF complex. Additionally, Pathway enrichment analyses of SEVs•Tat and SEVs•NF-ᴋB p65 complexes identifies biological functions involved in initiation of transcription and translation elongation at the HIV LTR, formation of HIV and RNA Pol II elongation complexes, protein, nucleic acid, and chromatin binding, as well as chromatin assembly and disassembly. Finally, integrative analysis of SEVs•Tat and SEVs•NF-ᴋB p65 binding proteins identifies four proteins (AKAP9, ARHGEF28, INTS1, BRD2) to be common to both complexes. Immunoprecipitation assays suggest that SEVs-associated BRD2 and NELFB bind HIV Tat. The identification of extracellular interactome of Tat and NF-κB p65 in HIV transcription paves the way for the rational design of novel inhibitors of HIV transcription, with potential for therapeutic targeting.

2026-06-15 | PXD062816 | Pride

Identification of HIV Tat and NF-kB binding proteins associated with semen derived extracellular vesicles In this study, we used orthogonal pull-downs, mobility shift, and electrophoretic protein binding assays coupled with proteomic and secretomic analyses to highlights the previously unappreciated SEV-associated transcriptional repressors that may target HIV Tat to suppress viral transcription.

2026-06-15 | PXD062784 | Pride

Human immunodeficiency virus 1

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Human Immunodeficiency Virus Tat Directly Interacts with a Specific Set of Cellular RNAs

Project description:We have used RNA immunoprecipitation to identify the set of mRNAs that HIV-1 Tat interacts with in T-cells. We have also performed measurements of relative RNA abundance to determine if Tat binding is associated with an increase in RNA abundance in Tat-expressing T-cells and during HIV infection of primary T-cells. We have also used RNA IP and ChIP-Chip to compare the RNAs with which Tat interacts with to the RNAs that RISC interacts with and the genes associated with pTEF-b.

2013-11-05 | E-MEXP-3199 | biostudies-arrayexpress

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Quantitative analysis of Tat-dependent and host-driven HIV transcription by ChIP-seq and RNA-seq

Project description:HIV transcription is initiated by host transcriptional machinery prior to the production of the viral transactivator Tat, yet the magnitude and regulatory features of this Tat-independent transcriptional state remain poorly defined. In this study, we performed integrated chromatin and transcriptional profiling to quantitatively compare Tat-dependent and host-driven regulation of HIV and cellular gene expression. Jurkat T cells were infected with isogenic HIV constructs expressing functional Tat (TatWT) or lacking Tat expression (TatNull) and analyzed under non-stimulated and stimulated conditions. Genome-wide chromatin occupancy of Tat and transcriptional machinery was measured by ChIP-seq, and corresponding transcriptional output from both the HIV provirus and host genome was quantified by RNA sequencing. These datasets define the baseline host-driven transcriptional state of HIV in the absence of Tat and enable direct comparison with Tat-amplified transcriptional responses. Together, this integrated ChIP-seq and RNA-seq resource provides a quantitative framework for dissecting Tat-dependent and Tat-independent mechanisms of HIV transcriptional regulation in chromatin.

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