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Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and interferon-α2a [RNA-seq]

ABSTRACT: Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and interferon-α2a [RNA-seq]

PROVIDER: PRJNA982154 | ENA |

REPOSITORIES: ENA

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Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and interferon-α2a [RNA-seq]

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.

2024-02-29 | GSE234623 | GEO

Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a [Cut&Run]

2024-02-29 | GSE234624 | GEO

Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a

Project description:Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a

| PRJNA982148 | ENA

Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a [Cut&Run]

Project description:Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and pegylated Interferon-⍺2a [Cut&Run]

| PRJNA982153 | ENA

Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and interferon-α2a.

Project description:CD4+ T cells with latent HIV-1 infection persist despite treatment with antiretroviral agents and represent the main barrier to a cure of HIV-1 infection. Pharmacological disruption of viral latency may expose HIV-1-infected cells to host immune activity, 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-α2a, 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 sites for panobinostat. By contrast, proviruses near H3K27ac marks were actively selected against, likely due to increased susceptibility to panobinostat. These data suggest that latency-reversing treatment can increase the immunological vulnerability of HIV-1 reservoir cells and accelerate the selection of epigenetically privileged HIV-1 proviruses.

| S-EPMC10903630 | biostudies-literature

Selection of epigenetically privileged HIV-1 proviruses during treatment with panobinostat and interferon-α2a

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

2024-02-29 | GSE234625 | GEO

Parallel analysis of transcription, integration, and sequence of single HIV-1 proviruses

Project description:HIV-1-infected cells that persist despite antiretroviral therapy (ART) are frequently considered ‘‘transcriptionally silent,’’ but active viral gene expression may occur in some cells, challenging the concept of viral latency. Applying an assay for proﬁling the transcriptional activity and the chromosomal locations of individual proviruses, we describe a global genomic and epigenetic map of transcriptionally active and silent proviral species and evaluate their longitudinal evolution in persons receiving suppressive ART. Using genome-wide epigenetic reference data, we show that proviral transcriptional activity is associated with activating epigenetic chromatin features in linear proximity of integration sites and in their inter- and intrachromosomal contact regions. Transcriptionally active proviruses were actively selected against during prolonged ART; however, this pattern was violated by large clones of virally infected cells that may outcompete negative selection forces through elevated intrinsic proliferative activity. Our results suggest that transcriptionally active proviruses are dynamically evolving under selection pressure by host factors.

2022-01-12 | GSE168337 | GEO

Bulk RNAseq of A375 cells treated with Panobinostat

Project description:The MICA and MICB genes are epigenetically regulated by HDACs. We tested if panobinostat, a broad spectrum HDAC inhibitor, affects the expression of MICA and MICB gene by a human melanoma cell line.

2020-02-19 | GSE145447 | GEO

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

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

Project description:The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression Neuroblastoma SK-N-BE(2) cells were treated with vehicle control, 1 microM JQ1, 10 nM panobinostat, or combination of JQ1 and panobinostat for 6 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

2015-12-31 | E-GEOD-68690 | biostudies-arrayexpress

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