Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277687 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transciptiome of human primary resting CD4 T lymphocytes infected with HIV-1
| PRJNA355967 | ENA
Project description:CD8+ and CD4+ T cells from HIV infected patients with HIV-RNA viremia
| PRJNA134707 | ENA
Project description:Host directed therapies against HIV-1 are thought to be critical for long term containment of the HIV-1 pandemic but remain elusive. Since HIV-1 infects and manipulates important effectors of both the innate and adaptive immune system, identifying modulations of the host cell systems in humans during HIV-1 infection may be crucial for the development of immune based therapies. Here, we quantified the changes of the proteome in human CD4+ T cells upon HIV-1 infection, both in vitro and in vivo. A SWATH-MS approach was used to measure the proteome of human primary CD4+ T cells infected with HIV-1 in vitro as well as CD4+ T cells from HIV-1 infected patients with paired samples on and off antiretroviral treatment. In the in vitro experiment, the proteome of CD4+ T cells was quantified over a time course following HIV-1 infection. 1,725 host cell proteins and 4 HIV-1 proteins were quantified, with 145 proteins changing significantly during the time course. Changes in the proteome peaked 24 hours after infection, concomitantly with significant HIV-1 protein production. In the in vivo branch of the study, CD4+ T cells from viremic patients and those with no detectable viral load after treatment were sorted and the proteomes quantified. We consistently detected 895 proteins, 172 of which were considered to be significantly different between viraemic patients and patients undergoing successful treatment. The proteome of in vitro infected CD4+ T cells was modulated on multiple functional levels, including TLR-4 signalling and the type 1 interferon signalling pathway. Perturbations in the type 1 interferon signalling pathway were recapitulated in CD4+ T cells from patients. The study shows that proteome maps generated by SWATH-MS indicate a range of functionally significant changes in the proteome of HIV infected human CD4+ T cells. Exploring these perturbations in more detail may help identify new targets for immune based interventions.
2017-02-28 | PXD005234 | Pride
Project description:Despite the success of antiretroviral therapy, HIV cannot be cured because of a reservoir of latently infected cells that evades therapy. To understand the mechanisms of HIV latency, we employed an integrated single-cell RNA-seq/ATAC-seq approach to simultaneously profile the transcriptomic and epigenomic characteristics of ~125,000 latently infected primary CD4 cells after reactivation using three different latency-reversing agents.
2023-12-28 | GSE242997 | GEO
Project description:Persistently infected macrophages serve as a long-term HIV reservoir and barrier to viral eradication, and also contribute to neurological complications in patients despite antiretroviral therapy (ART). To better understand the regulation of HIV in macrophages, we compared HIV infected human monocyte derived macrophages (MDM) to acutely infected primary CD4 T cells and Jurkat cell lines latently infected with HIV (JLAT). HIV genomes in MDM were actively transcribed despite enrichment with heterochromatin-associated H3K9me3 across the complete HIV genome in combination with elevated activation marks of H3K9ac and H3K27ac at the LTR. In contrast, JLAT showed conventional bivalent H3K4me3/H3K27me3 while CD4 showed an intermediate epigenotype. 5‘-methylcytosine (5mC) was enriched across the HIV genome in latently infected JLAT cells, while 5‘-hydroxymethylcytosine (5hmc) was enriched in CD4 and MDM. HIV infection induced multinucleation of MDMs along with DNA damage associate p53 phosphorylation, as well as loss of TET2 and the nuclear redistribution of 5-hydoxymethylation. RNA-seq analysis demonstrated that MDMs have a distinct transcriptional response to HIV persistent infection, including activation of CCL7, LAG3, and interferon signaling. Taken together, our findings suggest that HIV induces a unique macrophage nuclear and transcriptional profile, and viral genomes are maintained in a non-canonical bivalent epigenetic state.
2021-08-12 | GSE156072 | GEO
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:Single Cell RNA Sequencing in Primary CD4 T-Cells infected with HIV, suppressed with ART, and treated with IFNb
2022-06-01 | GSE176386 | GEO
Project description:HIV Nef Mediated Transcription in Primary CD4+ T cells
| PRJNA408146 | ENA
Project description:Sexually transmitted infections (STIs) are commonly reported among HIV-1 infected patients. The increasing prevalence of the most common STI, Chlamydia trachomatis (CT), among HIV-1 infected people suggests a role in HIV-1 infectivity. However, the mechanisms modulating the enhancement of HIV-1 infectivity during HIV-1/STIs coinfection remain elusive. The stimulation of CD4 T cells during CT infection may modulate the expression of specific genes, which in turn enhance the susceptibility and infectivity of CT-specific CD4 T cells to HIV-1 infection. After three days of CT stimulation of PBMCs followed by 3 days of HIV-1 infection, we observed a significant increase in HIV-1 p24 levels among clinically diagnosed C. trachomatis-infected patients as compared to cells from healthy donors. Similarly, ex vivo CT antigen-stimulated PBMCs from healthy donors showed enhanced susceptibility to HIV-1 as compared to unstimulated PBMCs. CT-specific CD4 T cells also harbour more HIV-1 copy numbers as compared to healthy unstimulated CD4 T cells. RNA-seq data revealed the upregulation of CCR chemokine receptors and cytokines in CD4 T cells from CT-stimulated CD4 T cells infected with HIV-1.
2021-12-31 | GSE164264 | GEO
Project description:Human Immunodeficiency Virus type-1 (HIV-1)-infected individuals show metabolic alterations of CD4 T cells through unclear mechanisms with undefined consequences. We analyzed the transcriptome of CD4 T cells from HIV-1 patients and revealed that elevated oxidative phosphorylation (OXPHOS) pathway is associated with poor outcomes. Inhibition of OXPHOS by the FDA-approved drug metformin, which targets mitochondrial respiratory chain complex I, suppresses HIV-1 replication in human CD4 T cells and humanized mice. In patients, HIV-1 peak viremia positively correlates with the expression of NLRX1, a mitochondrial innate immune receptor. Quantitative proteomics and metabolic analyses reveal that NLRX1 enhances OXPHOS and glycolysis during HIV-1-infection of CD4 T cells to promote viral replication. At the mechanistic level, HIV infection induces the association of NLRX1 with the mitochondrial protein, FASTKD5, to promote the expression of mitochondrial respiratory complex components. This study uncovers the OXPHOS pathway in CD4 T cells as a target for HIV-1 therapy.
2022-02-16 | PXD023565 | Pride