Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [RNA-seq]

ABSTRACT: The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [RNA-seq]

PROVIDER: PRJNA1021624 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26196890_1.fastq.gz	Fastqsanger.gz
	SRR26196890_2.fastq.gz	Fastqsanger.gz
	SRR26196891_1.fastq.gz	Fastqsanger.gz
	SRR26196891_2.fastq.gz	Fastqsanger.gz
	SRR26196892.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [Array]

Project description:Deciphering the mechanisms underlying viral persistence is critical to achieving a cure for HIV infection. Here, we implement a systems approach to discover molecular signatures of HIV latently-infected CD4+ T cells, identifying the immunosuppressive, adenosine-producing ectonucleotidase CD73 as a key surface marker of latent cells. Hypoxic conditioning, reflecting the lymphoid tissue microenvironment, increases the frequency of CD73+ CD4+ T cells and promotes HIV latency. Transcriptomic profiles of CD73+ CD4+ T cells favor viral quiescence, immune evasion, and cell survival. CD73+ CD4+ T cells are capable of harboring a functional HIV reservoir and reinitiating productive infection ex vivo. CD73 or adenosine receptor blockade facilitates latent HIV reactivation in vitro, mechanistically linking adenosine signaling to viral quiescence. Finally, tissue imaging of lymph nodes from HIV-infected individuals on antiretroviral therapy reveals spatial association between CD73 expression and HIV persistence in vivo. Our findings warrant development of HIV cure strategies targeting the hypoxia-CD73-adenosine axis.

2023-09-24 | GSE243577 | GEO

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [RNA-seq]

2023-09-28 | GSE244190 | GEO

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency

Project description:The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency

| PRJNA1021627 | ENA

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [Array]

Project description:The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency [Array]

| PRJNA1018954 | ENA

The hypoxia-regulated ectonucleotidase CD73 is a host determinant of HIV latency.

Project description: Not available

| S-EPMC10838153 | biostudies-literature

The Hypoxia-regulated Ectonucleotidase CD73 is a Host Determinant of HIV Latency

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

2023-09-28 | GSE244193 | GEO

Virus Entry is a Major Determinant of HCMV Latency in Monocytes

Project description:Virus Entry is a Major Determinant of HCMV Latency in Monocytes

| PRJNA1179887 | ENA

Expression data from CD73 positive adipose derived mesenchymal stem cells (CD73+ AD-MSCs) and CD73 negative adipose derived mesenchymal stem cells (CD73- AD-MSCs) of mouse

Project description:MSCs are a heterogeneous population and the specific population of MSCs may exhibit a selective ability for tissue repair. The aim of our research was to adapt the CD73+ subgroup of adipose derived MSCs (AD-MSCs) for the therapy of myocardial infarction (MI). Our results revealed that CD73+ AD-MSCs played more effective role in the acceleration function of cardiac recovery by promoting angiogenesis in a rat model of MI compared to mixed AD-MSCs and CD73- AD-MSCs. Microarray analysis shows differences between CD73+ and CD73- AD-MSCs when transcription profile of these two subgroups were compared, especially in VEGF pathway.

2021-06-02 | GSE167219 | GEO

PCID2 regulates HIV-1 transcription and viral RNA processing during latency

Project description:HIV-1 latency results from a combination of tightly regulated molecular processes that act at distinct steps of HIV-1 gene expression. In an effort to elucidate the molecular players that govern viral latency, we previously performed a dCas9 chromatin immunoprecipitation coupled with mass spectrometry (Catchet-MS) and identified proteins bound differentially to the latent LTR that putatively promote HIV-1 latency. Here we characterize the Catchet-MS identified PCI domain-containing 2 (PCID2) protein to play a dual role in promoting HIV-1 latency by enforcing both HIV-1 transcription repression as well as post-transcriptional blocks. PCID2 bound the latent HIV-1 LTR and repressed transcription initiation during latency. Depletion of PCID2 remodeled the chromatin landscape at the HIV-1 promoter and resulted in transcriptional activation and reversal of latency. Immunoprecipitation coupled to Mass Spectrometry identified the PCID2 interacting proteins to include members of the spliceosome and other splicing regulators, including negative regulators of viral RNA alternative splicing. PCID2 depletion resulted in over-splicing of intron-containing HIV-1 RNA and mis-regulated expression of vRNA splice variants. Finally, consistent with its role in NXF1-mediated nascent RNA nucleocytoplasmic export as part of the TREX2 complex, PCID2 modulates export of completely spliced vRNA. In summary, we demonstrate that PCID2 is a previously unidentified factor involved in HIV-1 latency regulation which plays a dual role in blocking HIV-1 gene expression by acting on transcription initiation as well as viral RNA processing.

2024-06-16 | PXD043334 | Pride

Glycolysis downregulation is a hallmark of HIV-1 latency and sensitizes infected cells to oxidative stress

Project description:HIV-1 infects lymphoid and myeloid cells, which can harbor a latent proviral reservoir responsible for maintaining lifelong infection. Glycolytic metabolism has been identified as a determinant of susceptibility to HIV-1 infection, but its role in the development and maintenance of HIV-1 latency has not been elucidated. By combining transcriptomic, proteomic and metabolomic analysis, we here show that transition to latent HIV-1 infection downregulates glycolysis, while viral reactivation by conventional stimuli reverts this effect. Decreased glycolytic output in latently infected cells is associated with downregulation of NAD+/NADH. Consequently, infected cells rely on the parallel pentose phosphate pathway and its main product, the antioxidant NADPH, fueling antioxidant pathways maintaining HIV-1 latency. Of note, blocking NADPH downstream effectors, thioredoxin and glutathione, favors HIV-1 reactivation from latency in lymphoid and myeloid cellular models. This provides a “shock and kill effect” decreasing proviral DNA in cells from people-living-with-HIV/AIDS. Overall, our data show that downmodulation of glycolysis is a metabolic signature of HIV-1 latency that can be exploited to target latently infected cells with eradication strategies.

2021-06-16 | GSE163979 | 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