Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355967 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RNA-Seq of HIV-infected human primary CD4+ T cells
| PRJNA277687 | ENA
Project description:Resting CD4+ T cells are infected by HIV-1 in vivo, however are refractory to cell-free HIV-1 infection in vitro. We show that they are efficiently infected by cell-to-cell spread. To allow resting T cell infection, uninfected resting target cells were co-cultured with infected donor T cells. Cells were infected with HIV-1 WT, dVpr or left mock treated and cultures with or without IL7. After 72h of co-culture, resting target cells were recovered by flow cytometry sorting and total RNA was extracted. RNASequencing revealed global transcriptomic reprogramming of resting memory T cells by HIV-1 Vpr.
2022-03-31 | E-MTAB-11454 | biostudies-arrayexpress
Project description:Comparison of total RNA-seq data from ex vivo unstimulated and stimulated (with anti-CD3/CD28) cells from two primary cell models of HIV latency (resting-cell and wild-type virus models) and peripheral CD4+ T cells from HIV-infected ART-suppressed individuals (ex vivo cells). Two donors were analyzed per model.
2020-10-28 | GSE144585 | 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
Project description:Using HIV-1 RNASortSeq, 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 eight antiretroviral therapy treated, virally suppressed, HIV-1-infected individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.
2021-04-01 | GSE112576 | GEO
Project description:Latently infected resting CD4+ T cells are a major barrier to HIV cure. Understanding how latency is established, maintained and reversed is critical to identifying novel strategies to eliminate latently infected cells. We demonstrate here that co-culture of resting CD4+ T cells and syngeneic myeloid dendritic cells (mDC) can dramatically increase the frequency of HIV DNA integration and latent HIV infection in non-proliferating memory, but not naïve, CD4+ T cells. Gene expression in non-proliferating CD4+ T cells, enriched for latent infection, showed significant changes in the expression of genes involved in cellular activation and interferon regulated pathways, including the down-regulation of genes controlling both NF-κB and cell cycle. We conclude that mDC play a key role in the establishment of HIV latency in resting memory CD4+ T cells, which is predominantly mediated through signalling during DC-T cell contact.
2014-11-01 | GSE52344 | GEO
Project description:Latently infected resting CD4+ T cells are a major barrier to HIV cure. Understanding how latency is established, maintained and reversed is critical to identifying novel strategies to eliminate latently infected cells. We demonstrate here that co-culture of resting CD4+ T cells and syngeneic myeloid dendritic cells (mDC) can dramatically increase the frequency of HIV DNA integration and latent HIV infection in non-proliferating memory, but not naïve, CD4+ T cells. Gene expression in non-proliferating CD4+ T cells, enriched for latent infection, showed significant changes in the expression of genes involved in cellular activation and interferon regulated pathways, including the down-regulation of genes controlling both NF-κB and cell cycle. We conclude that mDC play a key role in the establishment of HIV latency in resting memory CD4+ T cells, which is predominantly mediated through signalling during DC-T cell contact. Resting (CD69-CD25-HLA-DR-) CD4+ T cells were enriched from the blood of 4 normal donors by magnetic bead depletion and labelled with the proliferation dye SNARF. SNARFhiEGFP- CD4+ T cells cultured with (+DC) or without syngeneic bulk DC (lin-HLA-DR+), in the presence (HIV T) or absence (Mock T) of HIV, were sorted 5 days following infection with NL(AD8)-nef/EGFP (MOI 5).Culture media was supplemented with 10ng/mL of IL-7. The gene expression profile of the 4 cell populations: 1. HIV T (+DC); 2. Mock T (+DC); 3. HIV T; and 4. Mock T, was determined.
2014-11-01 | E-GEOD-52344 | biostudies-arrayexpress
Project description:Elite Long-Term Nonprogressors are asymptomatic HIV-infected individuals who display long-term virtually undetectable viremia, stable CD4 T cell counts and extremeley low levels of HIV reservoir, in the absence of antiretroviral therapy. We conducted a whole-genome transcriptional profiling study of sorted resting CD4 T cell subsets (naive, central memory, transitional memory and effector memory) in 7 Elite Long-Term Nonprogressors, 7 HIV-infected viremic and 7 uninfected individuals. HIV-1 cellular DNA levels were quantified in each sorted CD4 T cell subset
2015-01-10 | E-MTAB-1480 | biostudies-arrayexpress
Project description:The barrier to HIV-1 functional cure is caused by a small pool of latently infected resting CD4 T-cells that persist under antiretroviral therapy. Notably this latent reservoir of infected cells will produce replication-competent infectious virus once prolonged suppressive HAART is withdrawn. The reactivation of HIV-1 gene expression in T-cells harboring latent provirus in HIV-1 patients under HAART will likely result in depletion of this latent reservoir due to cytopathic effects and immune clearance. Many studies have investigated small molecules that reactivate HIV-1 gene expression but to date no latency reversal agent (LRA) has been identified to be specific, non-toxic, and effective in primary T-cells isolated from HIV-1 infected individuals undergoing long-term HAART. Stochastic fluctuations in HIV-1 tat gene expression have been attributed to be essential in the viral progression to latency. We hypothesized that exposing Tat to latently infected CD4 T-cells will result in potent latency reversal. Our results indicate the capacity of an engineered Tat to reactivate HIV-1 in latently infected cells from patients to a similar degree as the protein kinase C agonist PMA (Phorbol 12-Myristate 13-Acetate) while showing no T-cell activation nor any significant transcriptome perturbation in primary CD4 T-cells.
2023-09-05 | GSE235229 | GEO