Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents

ABSTRACT: Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents

PROVIDER: PRJNA369088 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5209790_1.fastq.gz	Fastqsanger.gz
	SRR5209790_2.fastq.gz	Fastqsanger.gz
	SRR5209800_1.fastq.gz	Fastqsanger.gz
	SRR5209800_2.fastq.gz	Fastqsanger.gz
	SRR5209810_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 102

Similar Datasets

Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents [LARA]

Project description:HIV-1 persists in individuals on ART in infected central (CM), transitional (TM) and effector memory (EM) CD4+ T cells. We developed LARA (latency and reversion assay), which facilitates the examination of HIV latency reversal in CM, TM and EM subsets in a single assay. Studies with latency reversing agents (LRAs) revealed responses specific to each subset, including compounds that significantly reversed latency in all subsets but with a range of efficiency (bryostatin) to those that demonstrated subset specificity (IL-15). Significantly, LARA has allowed the demonstration that EM cells display a more activated profile compared to CM, which translated to enhanced efficiency in responsiveness to multiple LRAs and allowed the identification of mechanisms associated with the compounds that reactivate latent HIV in all subsets. Understanding the responsiveness of memory CD4+ T cells subsets to LRAs will accelerate the development of anti-latency therapy to interfering with viral persistence in vivo.

2018-01-26 | GSE94149 | GEO

Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents [LRA stimulated]

2018-01-26 | GSE94150 | GEO

Defining the Effects of PKC Modulator HIV Latency-Reversing Agents on Natural Killer Cells

Project description:Defining the Effects of PKC Modulator HIV Latency-Reversing Agents on Natural Killer Cells

| PRJNA1214395 | ENA

Defining the Effects of PKC Modulator HIV Latency-Reversing Agents on Natural Killer Cells

Project description:Latency reversing agents (LRAs) such as protein kinase C (PKC) modulators can reduce rebound-competent HIV reservoirs in small animal models. Furthermore, administration of natural killer (NK) cells following LRA treatment improves this reservoir reduction. It is currently unknown why the combination of a PKC modulator and NK cells is so potent and whether exposure to PKC modulators may augment NK cell function in some way. Here, we compare the transcriptional profiles of PKC-treated NK and CD4+ T cells to assess their generalized cellular effects. Transcriptomic profiles from both cell types displayed signatures of cellular activation and enrichment of genes associated with the NFκB pathway. However, the transcriptomic effects of PKC stimulation on NK cells are much milder than that in CD4+ T cells. This finding, combined with our experimental data testing killing capacity of PKC-stimulated NK cells against K562 cells and infected CD4+ T cells suggests that their contribution in “kick and kill” strategies is primarily due to upregulating HIV expression in CD4+ T cells, rather than directly enhancing the effector functions of NK cells. This suggests that PKC modulators are primarily augmenting the “kick” rather than the “kill” arm of this HIV cure approach.

2025-01-23 | GSE287754 | GEO

NSC95397 is a Novel HIV Latency Reversing Agent

Project description:The latent viral reservoir represents one of the major barriers of curing HIV. Focus on the “kick and kill” approach, in which virus expression is reactivated then cells producing virus are selectively depleted, has led to the discovery of many latency reversing agents (LRAs) that can reactivate latently integrated virus and further our understanding of the mechanisms driving HIV latency and latency reversal. Thus far, individual compounds have yet to be robust enough to work as a therapy, highlighting the importance of identifying new compounds that target novel pathways and synergize with known LRAs. In this study, we identified a promising LRA, NSC95397, from a screen of ~4250 compounds in J-Lat cell lines. We validated that NSC95397 reactivates latent viral transcription and protein expression from cells with unique integration events. Co-treating cells with NSC95397 and known LRAs demonstrated that NSC95397 has the potential to synergize with different drugs under both standard normoxic and physiological hypoxic conditions. We showed that NSC95397 does not globally increase open chromatin, and bulk RNA sequencing revealed that NSC95397 does not greatly change cellular transcription. Instead, NSC95397 downregulates many pathways key to metabolism, cell growth, and DNA repair – highlighting the potential of these pathways in regulating HIV latency. Overall, we identified NSC95397 as a novel LRA that does not alter global transcription, that shows potential for synergy with known LRAs, and that may act through novel pathways not previously recognized for their ability to modulate HIV latency.

2024-08-31 | GSE241617 | GEO

Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents

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

2018-01-26 | GSE94152 | GEO

NSC95397 is a Novel HIV Latency Reversing Agent

Project description:NSC95397 is a Novel HIV Latency Reversing Agent

| PRJNA1008920 | ENA

Homo sapiens

Project description:Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents [LARA]

| PRJNA369086 | ENA

Homo sapiens

Project description:Memory CD4+ T cell subsets show differential responses to HIV latency reversing agents [LRA stimulated]

| PRJNA369087 | ENA

Integrated single-cell multiomic analysis of HIV latency reversal reveals novel regulators of viral reactivation

Project description:Despite the success of antiretroviral therapy, HIV cannot be cured because of a reservoir of latently infected cells that evades therapy. To understand the mechanisms of HIV latency, we employed an integrated single-cell RNA-seq/ATAC-seq approach to simultaneously profile the transcriptomic and epigenomic characteristics of ~125,000 latently infected primary CD4 cells after reactivation using three different latency-reversing agents.

2023-12-28 | GSE242997 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data