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

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

PROVIDER: PRJNA842095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19391500_1.fastq.gz	Fastqsanger.gz
	SRR19391500_2.fastq.gz	Fastqsanger.gz
	SRR19391501.fastq.gz	Fastqsanger.gz
	SRR19391502_1.fastq.gz	Fastqsanger.gz
	SRR19391502_2.fastq.gz	Fastqsanger.gz

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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.

2022-06-03 | GSE204756 | GEO

Distinct gene expression by expanded clones of quiescent memory CD4<sup>+</sup> 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 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 reveals 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 possibilities for eradication.

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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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Project description:CD4 T cells with latent HIV-1 infection persist despite treatment with currently available antiretroviral agents and represent the main barrier to a cure of HIV-1 infection. Pharmacological disruption of viral latency may increase the immunological vulnerability of HIV-1-infected cells, but the clinical efficacy of latency-reversing agents for reducing HIV-1 persistence remains to be proven. Here, we show in a randomized, controlled human clinical trial that the histone deacetylase inhibitor panobinostat, when administered in combination with pegylated interferon-a2a, induces a structural transformation of the HIV-1 reservoir cell pool, characterized by a disproportionate overrepresentation of HIV-1 proviruses integrated in ZNF genes and in chromatin regions with reduced H3K27ac marks, the molecular target site for panobinostat. In contrast, proviruses near H3K27ac marks appeared to be actively selected against, likely due to increased susceptibility to panobinostat. These data suggest that latency-reversing treatment with panobinostat can accelerate immune selection of HIV-1 proviruses.

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