HIV wtNDK, HIV m7NDK
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE1716 | GEO | 2005/04/13
SECONDARY ACCESSION(S): PRJNA90377
REPOSITORIES: GEO
Similar Datasets
Project description:Arrays analyses of CEM non infected and CEM infected by HIV wtNDK or HIV m7NDK (mutant). The arrays used were done at AECOM (ET arrays) and by affymetrix. They were hybridized with RNA of the cell lines infected or not. The analyses done as in bourdon et al. Cancer Res. 2002 Nov 1;62(21):6218-23, and with genesis. Keywords: parallel sample
2010-06-10 | E-GEOD-1716 | biostudies-arrayexpress
Project description:Herein expression trends of host miRNA were measured in HIV-1 latently infected and persistent replication cells, as well as the control cells. HIV-1 latency infection was established by infecting CEM-SS lymphocytes with HIV-1 Bru strain. After selection and long-term culture, the chronically infected cell showed the characteristics of latency definition: 1. The provirus was intergrated in to the host genome.2. No viral expression could be detected during culture.3 .Cell stimulators, such as TNFa,PMA, etc, reactivate the viral expression. As expected, miRNA trend was different in HIV-1 latency when compared to the control or HIV-1 replication. A subset of miRNAs is enriched in HIV-1 latency model. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate HIV-1 infection mode.
2012-12-01 | GSE38388 | GEO
Project description:Herein expression trends of host miRNA were measured in HIV-1 latently infected and persistent replication cells, as well as the control cells. HIV-1 latency infection was established by infecting CEM-SS lymphocytes with HIV-1 Bru strain. After selection and long-term culture, the chronically infected cell showed the characteristics of latency definition: 1. The provirus was intergrated in to the host genome.2. No viral expression could be detected during culture.3 .Cell stimulators, such as TNFa,PMA, etc, reactivate the viral expression. As expected, miRNA trend was different in HIV-1 latency when compared to the control or HIV-1 replication. A subset of miRNAs is enriched in HIV-1 latency model. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate HIV-1 infection mode. In this study, the in vitro steady cell culture was used to explore the miRNA transcription signatures in HIV-1 infection. miRNA profiles were performed and compared among normal control,HIV-1 latency and HIV-1 replication .
2012-12-01 | E-GEOD-38388 | biostudies-arrayexpress
Project description:Opioid use is associated with worse outcome in HIV-infected patients. The exacerbated disease progression by opioids is mainly driven by increased epithelial damage and less regenerative response. The present study investigates how opioids potentiate HIV disease progression by impairing intestinal epithelial self-repair. Abnormal intestinal morphology and reduced epithelial proliferation were observed in HIV-infected humanized mice, which were exposed to opioids. For this study, we had 4 groups of BLT humanized mice- (A) Untreated, (B) Morphine treated, (C) HIV infected and (D) HIV infected + Morphine treated. HIV infection was done for 4 weeks and Morphine treatment was done for 7 days. Morphine treatment was done via subcutaneous implantation of slow-release morphine pellet in individual mouse in the appropriate groups. In other groups, a matching Placebo pellet was implanted.
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2012-12-31 | E-GEOD-29507 | biostudies-arrayexpress
Project description:Viruses manipulate host cells to enhance their replication, and the identification of host factors targeted by viruses has led to key insights in both viral pathogenesis and cellular physiology. We previously described global changes in cellular protein levels during human immunodeficiency virus (HIV) infection using transformed CEM-T4 T cells as a model. In this study, we develop an HIV reporter virus displaying a streptavidin-binding affinity tag at the surface of infected cells, allowing facile one-step selection with streptavidin-conjugated magnetic beads. We use this system to obtain pure populations of HIV-infected primary human CD4+ T cells for detailed proteomic analysis, including quantitation of >9,000 proteins across 4 different donors, and temporal profiling during T cell activation. Remarkably, amongst 650 cellular proteins significantly perturbed during HIV infection of primary T cells (q<0.05), almost 50% are regulated directly or indirectly by the viral accessory proteins Vpr, Vif, Nef and Vpu. The remainder have not been previously characterised, but include novel Vif-dependent targets FMR1 and DPH7, and 192 targets not identified and/or regulated in T cell lines, such as AIRD5A and PTPN22. We therefore provide a high-coverage functional proteomic atlas of HIV infection, and a mechanistic account of HIV-dependent changes in its natural target cell.
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Project description:Genomic alteration of cervical cancer samples. Analysis by CGH array. Array spotted at AECOM (NY) with human ESTs. Analysis as in Bourdon et al. Cancer Res. 2002 Nov 1;62(21):6218-23 Keywords: parallel sample
2005-04-13 | GSE1715 | GEO
Project description:In this GEO submission we include the PA-m6A-seq and PA-m5C-seq datasets for HIV in CEM & 293T cells
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Project description:Illumina sequencing data used in HIV-CRISPR screen with an ISG-specific sgRNA library (PIKAHIV) to find genes that block infection by the N74D and P90A HIV-1 capsid mutant viruses in THP-1 monocytic cells. For more information on the library and approach see Ohainle et al. eLife 2018 (PMID: 30520725). All screens performed here were done in a clonal ZAP-KO cell line (ZAP may inhibit the HIV-CRISPR vector used in the screen). Here we screen the Cyclophilin A-binding deficient mutant P90A and the CPSF6-binding deficient mutant N74D together with a wild type HIV-1 virus. The N74D screen was performed both with IFN treatment and without. These two HIV-1 capsid mutant viruses are hypersensitive to the effects of IFN.
2019-11-16 | GSE140467 | GEO
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.
2020-05-15 | GSE126230 | GEO