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Transcription of HIV-1 at sites of intact latent provirus integration [scRNA-seq]

ABSTRACT: Transcription of HIV-1 at sites of intact latent provirus integration [scRNA-seq]

PROVIDER: PRJNA1114000 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29099400.fastq.gz	Fastqsanger.gz
	SRR29099401.fastq.gz	Fastqsanger.gz
	SRR29099402.fastq.gz	Fastqsanger.gz
	SRR29099403.fastq.gz	Fastqsanger.gz
	SRR29099404.fastq.gz	Fastqsanger.gz

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Transcription of HIV-1 at sites of intact latent provirus integration

Project description:Transcription of HIV-1 at sites of intact latent provirus integration

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Transcription of HIV-1 at sites of intact latent provirus integration [scRNA-seq]

Project description:The study examined proviral and neighboring gene transcription at sites of intact latent HIV-1 integration in cultured T cells obtained directly from people living with HIV, as well as engineered primary T cells and cell lines and showed that the site of integration has a dominant effect on the transcriptional activity of intact HIV-1 proviruses in the latent reservoir

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Transcription of HIV-1 at sites of intact latent provirus integration [ATAC-seq]

Project description:Transcription of HIV-1 at sites of intact latent provirus integration [ATAC-seq]

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Transcription of HIV-1 at sites of intact latent provirus integration.

Project description:HIV-1 antiretroviral therapy is highly effective but fails to eliminate a reservoir of latent proviruses, leading to a requirement for life-long treatment. How the site of integration of authentic intact latent proviruses might impact their own or neighboring gene expression or reservoir dynamics is poorly understood. Here, we report on proviral and neighboring gene transcription at sites of intact latent HIV-1 integration in cultured T cells obtained directly from people living with HIV, as well as engineered primary T cells and cell lines. Proviral gene expression was correlated to the level of endogenous gene expression under resting but not activated conditions. Notably, latent proviral promoters were 100-10,000× less active than in productively infected cells and had little or no measurable impact on neighboring gene expression under resting or activated conditions. Thus, the site of integration has a dominant effect on the transcriptional activity of intact HIV-1 proviruses in the latent reservoir, thereby influencing cytopathic effects and proviral immune evasion.

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Transcription of HIV-1 at sites of intact latent provirus integration

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-25 | GSE268010 | GEO

Chromatin maturation of the HIV provirus in primary resting CD4+ T cells

Project description:Human immunodeficiency virus (HIV) infection is a chronic condition, where viral DNA integrates into the genome. The fate of the provirus determines the infection course. Latently infected cells form a persistent, heterogeneous reservoir. The reservoir that reinstates an active infection comprises cells with intact provirus that can be reactivated. We confirmed that latent cells from patients exhibited active transcription throughout the provirus. To find transcriptional determinants, we characterized the establishment and maintenance of latency during proviral chromatin maturation in primary CD4+ T-cells for four months after HIV infection. As heterochromatin (marked with H3K9me3 or H3K27me3) gradually stabilized, the provirus became less accessible and lost activation potential. In a subset of infected cells, active marks (i.e., H3K27ac) remained detectable, even after prolonged proviral silencing. After T-cell activation, the proviral activation occurred uniquely in cells with H3K27ac-marked proviruses. Our observations suggested that, after transient proviral activation, cells were actively returned to latency.

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The chromatin landscape at the HIV-1 provirus integration site determines viral expression

Project description:We investigated the link between HIV-1 integration by using B-HIVE and LEDGINs. B-HIVE tracks insert-specific HIV expression by tagging a unique barcode in the HIV genome. LEDGINs are antivirals that inhibit the interaction between HIV-IN and its chromatin tethering cofactor LEDGF/p75. They are known to retarget HIV-1 integration sites. Here, we confirmed that LEDGIN treatment retargets integration out of transcriptionally active regions and reduce HIV expression. Silent provirus was located at increased distance to H3K36me3, the recognition marker of LEDGF/p75, after treatment with LEDGINs. Viral RNA expression was also influenced by the proximity of enhancers, regardless of the presence of LEDGINs.

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Distinct gene expression by expanded clones of quiescent memory CD4+ T cells harboring intact latent HIV-1 proviruses

Project description:Antiretroviral therapy controls but does not cure HIV-1 infection due to a reservoir of rare CD4 + T cells harboring latent proviruses. Little is known about the transcriptional program of latent cells. Here we report a novel strategy to enrich clones of latent cells carrying intact, replication-competent HIV-1 proviruses from blood based on their expression of unique T cell receptors. Latent cell enrichment enabled single cell transcriptomic analysis of 1,050 CD4 + T cells belonging to expanded clones harboring intact HIV-1 proviruses from 6 different individuals. The analysis revealed that most of these cells are T effector memory cells that are enriched for expression of HLA-DR, HLA-DP, CD74, CCL5, Granzymes A and K, cystatin F, LYAR and DUSP2. We conclude that expanded clones of latent cells carrying intact HIV-1 proviruses persist preferentially in a distinct CD4 + T cell population opening new possibilities for eradication.

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Project description:The chromatin landscape at the HIV-1 provirus integration site determines viral expression

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