Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (Bulk RNA-Seq)

ABSTRACT: HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (Bulk RNA-Seq)

PROVIDER: PRJNA954351 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24135502_1.fastq.gz	Fastqsanger.gz
	SRR24135502_2.fastq.gz	Fastqsanger.gz
	SRR24135503_1.fastq.gz	Fastqsanger.gz
	SRR24135503_2.fastq.gz	Fastqsanger.gz
	SRR24135504_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 54

Similar Datasets

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (scRNA-Seq)

Project description:HSV-2 coinfection is associated with increased HIV-1 viral loads and expanded tissue reservoirs, but the mechanisms are not well-defined. HSV-2 recurrences result in an influx of activated CD4+ T cells to sites of viral replication and an increase in activated CD4+ T cells in peripheral blood. We hypothesized that HSV-2 induces changes in these cells that facilitate HIV-1 reactivation and replication and tested this hypothesis in human CD4+ T cells and 2D10 cells, a model of HIV-1 latency. HSV-2 promoted latency reversal in HSV-2 infected and bystander 2D10 cells. Bulk and single-cell RNA sequencing studies of activated primary human CD4+ T cells identified decreased expression of HIV-1 restriction factors and increased expression of transcripts including MALAT1 that could drive HIV replication in both the HSV-2-infected and bystander cells. Transfection of 2D10 cells with VP16, an HSV-2 protein that regulates transcription, significantly upregulated MALAT1 expression, decreased trimethylation of lysine 27 on histone H3 protein, and triggered HIV latency reversal. Knockout of MALAT1 from 2D10 cells abrogated the response to VP16 and reduced the response to HSV-2 infection. These results demonstrate that HSV-2 contributes to HIV-1 reactivation through diverse mechanisms including upregulation of MALAT1 to release epigenetic silencing.

2023-05-07 | GSE229391 | GEO

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (Bulk RNA-Seq)

2023-05-07 | GSE229390 | GEO

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal

Project description:HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal

| PRJNA954346 | ENA

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (scRNA-Seq)

Project description:HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal (scRNA-Seq)

| PRJNA954353 | ENA

HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal.

Project description:Herpes simplex virus type 2 (HSV-2) coinfection is associated with increased HIV-1 viral loads and expanded tissue reservoirs, but the mechanisms are not well defined. HSV-2 recurrences result in an influx of activated CD4+ T cells to sites of viral replication and an increase in activated CD4+ T cells in peripheral blood. We hypothesized that HSV-2 induces changes in these cells that facilitate HIV-1 reactivation and replication and tested this hypothesis in human CD4+ T cells and 2D10 cells, a model of HIV-1 latency. HSV-2 promoted latency reversal in HSV-2-infected and bystander 2D10 cells. Bulk and single-cell RNA-Seq studies of activated primary human CD4+ T cells identified decreased expression of HIV-1 restriction factors and increased expression of transcripts including MALAT1 that could drive HIV replication in both the HSV-2-infected and bystander cells. Transfection of 2D10 cells with VP16, an HSV-2 protein that regulates transcription, significantly upregulated MALAT1 expression, decreased trimethylation of lysine 27 on histone H3 protein, and triggered HIV latency reversal. Knockout of MALAT1 from 2D10 cells abrogated the response to VP16 and reduced the response to HSV-2 infection. These results demonstrate that HSV-2 contributes to HIV-1 reactivation through diverse mechanisms, including upregulation of MALAT1 to release epigenetic silencing.

| S-EPMC10232005 | biostudies-literature

scRNASeq of HSV-1 latency

Project description:scRNASeq of HSV-1 latency

| PRJEB39022 | ENA

Stacking the odds: multiple sites for HSV-1 latency

Project description:investigated the possible contribution of various cells (i.e., B cells, DCs, fibroblasts, glial cells, ILCs, macrophages, microglia, monocytes, NK cells, neurons, neutrophils, and T cells) isolated from TG of latently infected mice to HSV-1 latency

2023-02-22 | GSE225839 | GEO

HSV-2 Triggers Upregulation of MALAT1 in CD4+ T cells and Promotes HIV Latency Reversal

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

2023-05-07 | GSE229392 | GEO

CaptureSeq to study HIV-1 transcription after reversal of latency

Project description:The goal of this study was to utilize CaptureSeq to be able to measure HIV-1 transcription after reversal of latency in primary cells from antiretroviral-treated HIV-1 infected individuals.

2021-06-01 | GSE152377 | GEO

POTENT LATENCY REVERSAL BY TAT RNA ENABLES IN-DEPTH MULTI-OMIC ANALYSIS OF THE TRANSLATION-COMPETENT HIV RESERVOIR

Project description:HIV infection remains incurable due to the long-term persistence of latently infected cells, capable of refueling viremia upon antiretroviral therapy interruption. Shock-and-kill strategies aim to purge this latent reservoir by inducing the expression of viral genes, making infected cells visible for cleanup by the immune system. Here, we present a Tat mRNA formulation that, when combined with panobinostat, enables latency reversal at levels >3-fold higher than those reached with the most potent mitogens. We demonstrate that this mRNA formulation does not alter the transcriptome or phenotype of CD4 T cells, enabling the ex vivo assessment of infected cells upon latency reversal in a near-native state. Taking advantage of this characteristic, we show transcriptomic and proteomic differences between infected cells upon latency reversal and non-infected cells, including the upregulation of the cytotoxic protein granzyme A and a novel long non-coding RNA. Overall, we demonstrate that a Tat mRNA formulation enables potent reactivation of latent HIV, presenting a valuable research tool for studying the inducible HIV reservoir, as well as paving the way to a more effective shock-and-kill functional cure.

2023-11-09 | GSE247402 | 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