Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis to examine glycan-related gene expression in primary human cells infected with HIV-1

ABSTRACT: The main objective of my laboratory is to identify the molecular mechanisms of HIV-1 entry and infection of the CNS, focusing on PG-species as the primary attachment receptors, and their interactions with certain HIV-1 proteins. Microarray analysis to examine glycan-related gene expression in primary human cells infected with HIV-1 to confirm that distinct cell-associated PGs play differential role(s) in viral capture and transfer via BMVECs and astrocytes To examine glycan-related gene expression in primary human cells (CNS-based cells such as BMVECS, astrocytes and microglia, as well as primary human control peripheral blood mononuclear cells, such as CD4+ T-cells and macrophages) infected with HIV-1 at different time-points (6 hours post-infection, 24-hours post-infection and 7-days post-infection) as compared to uninfected cells (all of the above cells, uninfected, in triplicates, with matching time-points).

ORGANISM(S): Homo sapiens

SUBMITTER: Steven Head

PROVIDER: E-GEOD-29939 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Differentially Expressed Pseudogenes in HIV-1 Infection

Project description:We analyzed transcriptomic data from infected and uninfected T-cells to identify pseudogenes and their parent genes showing differential expression in HIV-1 infection H9 T-cell line was infected with NL4-3 strain of HIV-1 obtained by transfection of 293T cells. RNA from infected and uninfected cells was extracted 7 days post infection.

2016-02-29 | E-GEOD-70785 | biostudies-arrayexpress

Differentiation of human fetal multipotential neural progenitor cells to astrocytes reveals susceptibility factors for JC Virus

Project description:Viral infections of the CNS are of increasing concern, especially among immunocompromised populations. Rodent models are often inappropriate for studies of CNS infection, as many viruses, including JC Virus (JCV) and HIV, cannot replicate in rodent cells. Consequently, human fetal brain-derived multipotential CNS progenitor cells (NPCs) that can be differentiated into neurons, oligodendrocytes, or astrocytes, have served as a model for CNS studies. NPCs can be non-productively infected by JCV, while infection of progenitor-derived astrocytes (PDAs) is robust. We profiled cellular gene expression at multiple times during differentiation of NPCs to PDAs. Several activated transcription factors show commonality between cells of the brain in which JCV replicates and lymphocytes in which JCV is likely latent. Bioinformatic analysis determined transcription factors that may influence the favorable transcriptional environment for JCV in PDAs. This study attempts to provide a framework for understanding the functional transcriptional profile necessary for productive JCV infection. 19 Human samples: 4 Human Fetal Brain NPC 0h, 4 Human Fetal Brain NPC in Serum 1h, 4 Human Fetal Brain NPC in Serum 1d, 4 Human Fetal Brain NPC in Serum 7d, 3 Human Fetal Brain NPC in Serum 30d.

2013-04-09 | E-GEOD-43794 | biostudies-arrayexpress

Single-cell TCR profiling of CSF and blood cells of PWH reveals persistent and shared infected T cell clones across tissue compartments even after ART

Project description:The brain is a site of persistent infected cells during HIV infection. However, the dynamics of central nervous system (CNS) infection and T cell trafficking in people living with HIV (PWH) are incompletely understood. We profiled the single cell T cell repertoire and host transcriptome from paired blood and cerebrospinal fluid (CSF) from PWH and uninfected controls. We detected HIV RNA-producing cells in 8/11 (72.7 %) CSF samples and 6/11 (54.5 %) blood samples, with a higher frequency of infected single CD4 T cells in CSF than in blood. Infected CSF T cells displayed a unique transcriptional profile compared to uninfected CSF T cells. Most infected T cell clones were not shared across tissue; however, in a subset of participants we detected identical T cell clones that were infected in both CSF and blood. Longitudinally following one PWH before and at three time points after initiating ART, we found infected T cell clones that persisted after ART initiation, in both CSF and blood, including a T cell clone that expanded in the CSF several months after ART initiation. Our findings suggest that infected T cells traffic to the CNS where they undergo clonal expansion despite ART, contributing to the CNS reservoir.

2024-04-15 | GSE243905 | GEO

Transcription profiling of monkey model of neuroAIDS reveals induction of pathogenic sets of genes in macrophages and neurons

Project description:The etiology of the central nervous system (CNS) alterations after human immunodeficiency virus (HIV) infection, such as dementia and encephalitis, remains unknown. We have used microarray analysis in a monkey model of neuroAIDS to identify 98 genes, many previously unrecognized in lentiviral CNS pathogenesis, whose expression is significantly up-regulated in the frontal lobe of simian immunodeficiency virus-infected brains. Further, through immunohistochemical illumination, distinct classes of genes were found whose protein products localized to infiltrating macrophages, endothelial cells and resident glia, such as CD163, Glut5, and ISG15. In addition we found proteins induced in cortical neurons (ie, cyclin D3, tissue transglutaminase, 1-antichymotrypsin, and STAT1), which have not previously been described as participating in simian immunodeficiency virus or HIV-related CNS pathology. This molecular phenotyping in the infected brains revealed pathways promoting entry of macrophages into the brain and their subsequent detrimental effects on neurons. These data support the hypothesis that in HIV-induced CNS disease products of activated macrophages and astrocytes lead to CNS dysfunction by directly damaging neurons, as well as by induction of altered gene and protein expression profiles in neurons themselves which are deleterious to their function.

2008-06-12 | E-GEOD-2377 | biostudies-arrayexpress

Differentiation of human fetal multipotential neural progenitor cells to astrocytes reveals susceptibility factors for JC Virus

2013-04-09 | GSE43794 | GEO

Microarray analysis to examine glycan-related gene expression in primary human cells infected with HIV-1

Project description:The main objective of my laboratory is to identify the molecular mechanisms of HIV-1 entry and infection of the CNS, focusing on PG-species as the primary attachment receptors, and their interactions with certain HIV-1 proteins.

2011-06-14 | GSE29939 | GEO

Methamphetamine increases the proportion of SIV-infected microglia/macrophages, alters metabolic pathways, and elevates cell death pathways: a single-cell analysis

Project description:Both drugs abuse and HIV infection continue to affect many indiviiduals. Both have untoward effects on the brain, and the two conditions often co-exist. In the brain, macrophages and microglia are infectable by HIV, and these cells are also targets for the effects of drugs of abuse such as the psychostimulant methamphetamine. In order to determine the interaction of HIV and methamphetamine we isolated microglia and macrophages from the brains of SIV-infected rhesus monkeys treated with methamphetamine and from SIV-infected monkeys who did not receive methamphetamine. Cells were subjected to single cell RNA sequencing and results analyzed by statistical and bioinformatic analysis. In the animals treated with methamphetamine, a significantly increased proportion of cells were infected by SIV. In addition, genes encoding functions in cell death pathways were increased, and the brain-derived neurotropic factor pathway was inhibited. The gene expression patterns in infected cells did not cluster separately from uninfected cells, but clusters comprised of cells from methamphetamine-treated animals differed in neuroinflammatory and metabolic pathways from those comprised of cells from untreated animals. Methamphetamine increases CNS infection by SIV and has adverse effects on both infected and uninfected microglia and brain macrophages, highlighting the dual and interacting harms of HIV infection and drug abuse on the brain.

2020-12-01 | GSE160384 | GEO

Transcription profiling of human CD4+/CD8+ T cells obtained from HIV patients at various stages of disease vs. uninfected individuals reveals HIV infection induces a persistent T cell transcriptional profile

Project description:We examined the gene expression profiles in ex vivo human CD4+ and CD8+ T cells from untreated HIV-infected individuals at different clinical stages and rates of disease progression. Profiles of pure CD4+ and CD8+ T cells subsets from HIV-infected nonprogressors who controlled viremia were indistinguishable from HIV-uninfected individuals. Similarly, no gene clusters could distinguish T cells from individuals with early from chronic progressive HIV infection, whereas differences were observed between uninfected or nonprogressors versus early or chronic progressors. In early/chronic HIV infection, three characteristic gene expression signatures were observed: (1) CD4+ and CD8+ T cells showed increased expression of interferon stimulated genes (ISGs). However, some ISGs including CXCL9, CXCL10, and CXCL11, and the IL15R? in both CD4+ and CD8+ T cells and the anti-HIV ISG APOBEC3G in CD4+ T cells, were not upregulated. (2) CD4+ and CD8+ T cells showed a cluster similar to that observed in thymocytes, and (3) more genes were differentially regulated in CD8+ T cells than in CD4+ T cells, including a cluster of genes downregulated exclusively in CD8+ T cells. In conclusion, HIV infection induces a persistent T cell transcriptional profile, early in infection, characterized by a dramatic but potentially aberrant interferon response, and a profile suggesting an active thymic output. We studied a cohort of HIV infected individuals with various clinical stages of HIV infection and healthy uninfected volunteers as a control group (Table 1). We included 5 individuals with early HIV infection (A), five with chronic progressive HIV infection (C), five individuals with non-progressive HIV infection with low or undetectable viral loads (L) and five HIV uninfected individuals (N). The HIV infected individuals were never on therapy prior to entering the study. Samples were taken once from each donor.

2007-11-11 | E-GEOD-6740 | biostudies-arrayexpress

Insights into responses of human astrocytes to H5N1 infection by transcriptional analysis

Project description:Increasing evidence demonstrates influenza virus can not only affect the respiratory system, but also infect CNS and lead to CNS disorder and encephalopathy and encephalitis. Astrocytes are the most abundant cells in the CNS, which are capable of producing cytokines and neurotrophic factors and are essential for brain homeostasis and neuronal function. Previous studies suggested that influenza virus can infect astrocytes and induce proinflammatory cytokines response as well as apoptosis. Nevertheless, very few mechanistic data are available regarding host responses to H5N1 infection in astrocytes. In this study, a functional genomics approach was utilized to investigate comprehensive host responses to H5N1 infection in a human astrocyte cell line, U251 cells. U251 cells were infected by H5N1 at MOI 1 or control . At time points 6, 12, and 24h, total RNA were extracted for microarray experiment. Three replicates were performed at each time point of infection and control infection.

2016-01-04 | E-GEOD-66597 | biostudies-arrayexpress

Induction of IL-17+ T-cells by HIV-Tat protein is mediated via Vascular Endothelial Growth Factor Receptor-2

Project description:Anti-retroviral therapy (ART) has transformed human immunodeficiency virus (HIV) infection from a fatal illness to a chronic condition by controlling viral replication and restoring immune function. However, chronic T-cell activation can be observed in 20-35% of individuals on ART, resulting in an immune reconstitution inflammatory syndrome (IRIS) [1-3]. IRIS involving the CNS can result in permanent disability and death [4]. Tat is a viral protein produced in HIV-infected cells and released into the extracellular space [5]. We show that the secreted-Tat protein activated uninfected T-cells in an antigen-independent manner without inducing proliferation. Notably, Tat induced the secretion of IL-17 from T-cells and increased the percentage of T-cells with a Th17 phenotype. T-cell activation was independent of the T-cell receptor but dependent on endocytosis of Tat and activation of vascular endothelial growth factor receptor 2 (VEGFR2). Tat induced global changes in histone acetylation and increased HIV infection in non-replicating T-cells. Furthermore, in an individual with CNS IRIS, Tat expressing infiltrates and secretion of IL-17 was detected in the absence of viral replication in the brain. Thus Tat can induce T-cell activation in a paracrine and autocrine manner resulting in propagation of inflammation and increased virulence. 12 Human samples in 6 pairs: 6 Human T cell HIV tat exposed 0hrs, 6 Human T cell HIV tat exposed 24hrs

2013-08-02 | E-GEOD-44460 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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