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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE318861 | GEO | 2026/07/01

REPOSITORIES: GEO

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Project description:Our previous work demonstrated that HIV-1 infection progressively reduces TCR/CD3 expression due to a defect in CD3g gene transcripts. We further found that knocking down expression of the viral tat and/or nef genes was correlated with CD3g transcript and TCR/CD3 surface receptor levels on HIV-1 infected cells. This study was undertaken to investigate the direct effect of HIV-1 Tat expression on the TCR/CD3 machinery. Progressive downregulation from TCR/CD3hi to TCR/CD3lo to TCR/CD3â was observed on Tat expressing cells in a manner that emulated HIV-1 infection, with a lack of CD3g transcripts again responsible for the defect. When Tat cell cultures containing a mixture of TCR/CD3 surface densities were separated into TCR/CD3hi and TCR/CD3lo/â populations, they quickly reverted to a mixed CD3 phenotype. Thus, the progression TCR/CD3hi to TCR/CD3lo to TCR/CD3â is an active, reversible process with receptor levels fluctuating in response to intracellular dynamics. Examination of tat mutants found that the regions involved in Tat-mediated transactivation and TAR binding are required for TCR/CD3 downregulation while the lysine at position 28 and Tat exon 2 are dispensable. Global gene expression, assessed in association with TCR/CD3 downregulation in HIV-1 infected and Tat expressing cells, detected broad suppression of TCR/CD3 signaling, co-stimulation and negative regulatory genes along with target transcription factors, ligands and receptors. A significant subset of the genes altered in HIV-1 infected cells was specifically targeted by Tat in association with TCR/CD3 loss. Our finding that Tat negatively regulates many facets of the TCR/CD3 machinery has important implications for disease pathogenesis. We used microarrays to investigate changes in CD4+ T cell gene expression induced by expression of the HIV-1 Tat protein. Examine changes in gene expression in HIV-1 Tat transduced cells compared with cells transduced with an antisense Tat sequence used as a control.

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

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