Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of keratinocytes laser captured from skin biopsies during the mucocutaneous HSV-2 reactivation

ABSTRACT: We aim to analyze the transcriptional profiles of keratinocytes near dermal-epidemal junction during HSV-2 reactivation in humans, including lesion, post healed (4 and 8 weeks post healing) and contra-lateral control biopsies. Since keratinocytes are the main target cells for HSV-2 infection, the goal is to define the intrinsic immunity of keratinocytes during HSV-2 reactivation in humans.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98540 | GEO | 2017/05/05

SECONDARY ACCESSION(S): PRJNA385479

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide analysis of CD8 cells laser captured from skin biopsies during the mucocutaneous HSV-2 reactivation

Project description:Analysis of CD8 cells at the gene expression level during the genital HSV-2 reactivation. We would like to get a comprehensive overview on gene expression of CD8 T-cells during the post healing phases of HSV-2 reactivation. The hypothesis is that CD8 T-cells play a immune surveillance function during the post healing phases. CD8 cells were immunofluorescently stained and laser captured from post healing biopsies and contralateral control biopsies, total RNA were purified from captured cells and cDNA were amplified from the total RNA using NuGEN pico kits

2012-07-25 | E-GEOD-39625 | biostudies-arrayexpress

Transcriptional profiling of CD8 cells laser captured from skin biopsies at dermal-epidermal junction and at deeper dermal area near blood vessel during the healed phase of mucocutaneous HSV-2 reactivation

Project description:We aim to get a comprehensive analysis on gene expression of CD8a+ T-cells during the post healed phases of HSV-2 reactivation at different anatomic location (CD8a+ cells at dermal-epidermal junction versus CD8a+ cells in deeper dermal area near blood vessel). Our hypothesis is that JC_CD8 cells may function as a resident effector-like T-cells while BV_CD8 cells may be infiltrating cells from circulation. CD8 cells were immunofluorescently stained and laser captured from genital skin biopsies at dermal-epidermal junction at 2 and 8 weeks post healed (JC_2wks_CD8 and JC_8wks_CD8) and at deeper dermal area near blood vessel (BV_2wks_CD8 and BV_8wks_CD8); total RNA were purified from captured cells and cDNA were amplified from the total RNA using NuGEN pico kits

2013-04-11 | E-GEOD-44975 | biostudies-arrayexpress

Genome-wide analysis of CD8 cells laser captured from skin biopsies during the mucocutaneous HSV-2 reactivation

2012-07-26 | GSE39625 | GEO

2013-04-11 | GSE44975 | GEO

Genome-wide analysis of skin biopsies during the mucocutaneous HSV-2 reactivation

Project description:Analysis of host response at the gene expression level during the genital HSV-2 reactivation. We would like to get a comprehensive overview on host gene expression and correlate them with the infiltrated immune cell types during HSV-2 reactivation. The hypothesis is that HSV-2 may evade some aspects of host immune response during the recurrent infection.

2009-10-15 | GSE18527 | GEO

Human cellular models for Herpes Simplex Virus, type 1 (HSV-1) using induced pluripotent stem cell derived neuronal lineages

Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitro model to investigate molecular details of the mechanisms underlying latency and reactivation in human neurons. Induced pluripotent stem (iPS) cell technologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neural progenitor cells (NPCs) and neurons, which displays the main hallmarks of latency defined in animal models and in humans. Induced pluripotent stem (iPS) cells were generated from human skin biopsy samples

2014-05-02 | E-GEOD-46041 | biostudies-arrayexpress

Induced pluripotent stem cell derived neuronallineages as human cellular models for Herpes Simplex Virus, type 1 (HSV-1) infections

Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitromodel to investigate molecular details of the mechanisms underlying quiescence and reactivation in human neurons. Induced pluripotent stem (iPS) celltechnologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neurons, which displays the main hallmarks of latency defined in animal models and in humans. Our results show for the first time that: i) persistent infection cannot be established in neural progenitor cells (NPCs); ii) the ability of HSV-1 to establish persistent infection is extended to glutamatergic neurons, and not limited to sensory neurons; iii) in neuronal cultures persistently infected with HSV-1, viral genome is localized at the nuclear periphery; iv) HSV-1 acute infection reduces RNA editing at the GluRB site. These results highlight the importance of iPS-based platforms to elucidate unknown aspects of HSV-1 quiescence in human neurons. NPCs were 70-80% confluence

2014-05-02 | E-GEOD-46042 | biostudies-arrayexpress

Transcriptional profiling of human genital skin biopsies at lesion, 2- and 8-weeks post healing and contra-lateral control genital skin biopsies during recurrent HSV-2 infection

Project description:Analysis of host response at the gene expression level during lesion and post healing periods (2- & 8-weeks after HSV-2 reactivation induced lesion is resolved). We would like to get a comprehensive overview on host gene expression of genital skin during lesion and post healing periods of recurrent HSV-2 infection as compared to those in control skin.

2021-04-21 | GSE172423 | GEO

Transcriptional profiling of primary human keratinocytes treated with interferon gamma and/or infected with HSV-2 using Illumina beadarray

Project description:We aim to analyze the transcriptional profiles of primary human keratinocytes in response to interferon gamma (IFNG) treatment and/or HSV-2 (strain HG-52) infection. The goal is to define IFNG regulated intrinsic immunity of primary human keratinocytes and how HSV-2 infection regulates the intrinsic immunity of primary human keratinocyte.

2021-04-21 | GSE172424 | GEO

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

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