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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Assessment of RNA samples from macrophages infected or non-infected with HIV to determine the effect of HIV infection on the gene expression

ABSTRACT: We previously looked the differences in glyco genes using the CFG microarray in normal macrophages and T cells, in conjunction with our studies on effects of glycosylation on HIV/SIV infectivity. In the review of a submitted manuscript, the question arose on the effect of HIV infection on the gene expression. To address this interesting question, we looked at RNA samples derived from macrophages (derived from the sample donor), either infected or not with HIV (in vitro) at different time points. RNA preparations of infected and un-infected Human macrophage at three different time points (5, 7, and 10 days)were sent to the Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Steven Head

PROVIDER: E-GEOD-28944 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Assessment of RNA samples from macrophages infected or non-infected with HIV to determine the effect of HIV infection on the gene expression

Project description:We previously looked the differences in glyco genes using the CFG microarray in normal macrophages and T cells, in conjunction with our studies on effects of glycosylation on HIV/SIV infectivity. In the review of a submitted manuscript, the question arose on the effect of HIV infection on the gene expression.

2011-04-29 | GSE28944 | GEO

Fibrocytes differ from macrophages but can be infected with HIV-1

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2015-07-28 | E-GEOD-71290 | biostudies-arrayexpress

Fibrocytes differ from macrophages but can be infected with HIV-1

2015-07-28 | GSE71290 | GEO

HIV-1 infected Cell Pellets and Biotinylated Cannabidiol LC-MS/MS

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2022-04-04 | PXD027263 | Pride

HIV-1 SortSeq identifies HIV-1-infected cells from HIV-1-infected individuals

Project description:Using HIV-1 SortSeq, we identified HIV-1-infected cells containing inducible HIV-1 for RNAseq from resting CD4+ T cells treated with PMA/ionomycin for 16 hours from HIV-1-infected, antiretroviral therapy treated, virally suppressed individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.

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HIV-1 SortSeq identifies HIV-1-infected cells from HIV-1-infected individuals

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Inhibition of cathepsin B and SAPC secreted by HIV-infected macrophages reverse common and unique apoptosis pathways

Project description:Human immunodeficiency virus 1 (HIV-1) infects blood monocytes that cross the blood-brain barrier to the central nervous system inducing neuronal damage. This damage is prompted by the secretion of viral and neurotoxic factors by HIV-infected macrophages and can result in HIV associated neurocognitive disorders (HAND). One of these neurotoxic factors secreted by HIV-infected macrophages is cathepsin B (CATB), a lysosomal cysteine protease that plays an important role in neurodegeneration. CATB interacts with Serum Amyloid P component (SAPC) contributing to HIV-induced neurotoxicity. However, the neuronal apoptosis pathways triggered by CATB and SAPC remain unknown. We aimed to elucidate these pathways in neurons exposed to HIV-infected macrophage conditioned media (MCM) before and after inhibition of CATB or SAPC using Tandem Mass Tag (TMT) proteomics labeling. Based on significant fold change (FC) ≥ ǀ2ǀ and p-value < 0.05 criteria, a total of 10, 48 and 13 proteins were deregulated after inhibiting CATB, SAPC antibodies and the cathepsin B inhibitor CA-074, respectively. We found that antibodies against CATB and SAPC, as well as the CATB inhibitor CA-074 downregulated apoptosis related proteins. CATB, SAPC or apoptotic related proteins could become potential targets against HIV-induced neuronal degeneration.

2022-01-20 | PXD024636 | Pride

Expression data from in vitro HIV-1-infected macrophages responding to phagocytic stimuli

Project description:We used microarrays to detail the global programme of gene expression in human macrophages infected in vitro with HIV-1 and then subjected to phagocytic stimuli; we identified distinct classes of differentially regulated genes during this process Primary human macrophages from 3 different donors were infected with HIV-1ADA WT or mock-infected for 8 days. They were incubated or not (basal) with IgG-SRBCs (FcR) or Salmonella Typhimurium (4/74 strain) during 1 hour at 37Â°C, then lysed and RNA of each sample was analyzed with microarrays.

2016-07-03 | E-GEOD-59991 | biostudies-arrayexpress

Identification of Glycoproteins Associated with HIV Latently Infected Cells Using Quantitative Glycoproteomics

Project description:HIV infection is not curable due to viral latency. Compelling reports studying proteins such as CD2, PD-1, LAG-3 and TIGIT suggest that there is a distinct profile of surface proteins that can be used for targeting latently infected cells. We have recently reported that glycoproteins were differentially secreted from HIV latently infected ACH-2 cells compared to the parental A3.01 cells. This observation suggests that glyco-phenotype might be different in these two cell lines. To determine the difference, the ACH-2 and A3.01 cell lines were subjected to a glycoproteomic analysis. A total number of 940 unique N-linked glycosite-containing peptides from 515 glycoproteins were identified. Among the glycoproteins, 365 and 104 were annotated as cell surface and membrane-associated proteins, respectively. Label free quantitative LC-MS/MS analysis revealed a change of 236 glycosite-containing peptides from 172 glycoproteins between the two cell lines without reactivation. Bioinformatic analysis suggests that cell adhesion, immune response, glycoprotein metabolic process, cell motion and cell activation were associated with the changed proteins. After reactivation of latency by phorbol myristate acetate (PMA), changes in glycosite-containing peptides were observed in both cell lines. Changes in 49 glycosite-containing peptides from 45 glycoproteins might be due to viral replication. The changed proteins suggest that cell migration, response to wounding and immune response were impaired in reactivated latently infected cells. Our study provides important glycoproteomic data in respect to HIV latently infected cells. Glycoproteomics merits future application using primary cells to discover reveal mechanisms in HIV pathogenesis.

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Expression analysis of microRNAs in plasma of new HIV-infected cases, old HIV-infected cases and healthy controls.

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