Multiomics profiling of HIV-infected cells
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ABSTRACT:
PROVIDER: PRJNA764194 | ENA |
REPOSITORIES: ENA
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Project description:The restructuring of chromatin architecture following lentiviral integration is not well elucidated. We jointly interrogate (HIV-distal & -local) chromatin organization (via Hi-C & ATAC-seq) and the RNA landscape around defined sites of proviral integration using HIV-inducible cellular models. We report chromatin interaction networks and nuclear ultrastructure around integrated HIV-1 are predominantly preserved, suggesting HIV integration does not induce large scale remodeling of cellular chromatin. Instead, we find that induction of proviral transcription leads to stark local changes in nucleosome organization with chromatin accessibility increasing at the intergenic junction between the HIV-1 3’ LTR and flanking cellular genome. This result suggests subtle changes in chromatin structure may be mediating proviral activation. Using long-read Nanopore RNA-seq, we interrogate the local host & HIV transcriptomes, observing a small fraction of HIV-1 transcripts are chimeric read-through products, where transcription initiates at the HIV-1 5’ LTR promoter and continues extensively into the flanking cellular genome. Despite provirus-driven read-through, HIV-1 appears to have only a modest effect on the local transcriptional environment. The changes in chromatin accessibility and read-through at activated proviruses closely resembles lytic Herpes simplex virus type 1 (HSV-1) induced cellular chromatin reprogramming. We propose chromatin “opening” at the 3’ LTR HIV-host junction is important for sustained proviral activity, and overall, HIV proviruses do not significantly alter local host transcription and chromatin structure. Our studies provide the first in-depth integrative investigation of 3D chromatin organization, nucleosome density, and HIV-host transcriptomes at HIV-host genic boundaries.
2021-10-26 | GSE184345 | GEO
Project description:human primary monocytes purified from 2 healthy blood donors were infected in vitro with Zika virus or HIV for 48 hours. Proteomics profiling of infected versus non infected cells was performed to identify up/down-regulated proteins associated to the infection
2019-08-22 | PXD014002 | Pride
Project description:This study examine the transcriptional profiling of HIV dual reporter non-infected, latetnly infected and productively infected Jurkat T cells.
2021-01-21 | GSE149492 | 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:The clonal expansion of HIV-1-infected CD4+ T cells is a major barrier to cure. Using single-cell ECCITE-seq, we examined the transcriptional landscape, upstream immune regulators, HIV-1 RNA expression, and T cell clonal expansion dynamics of 215,458 CD4+ T cells (267 HIV-1 RNA+ cells and 68 expanded HIV-1 RNA+ T cell clones) from six HIV-1-infected individuals (during viremia and after suppressive antiretroviral therapy) and two uninfected individuals, in unstimulated conditions and after CMV and HIV-1 antigen stimulation. We found that despite antiretroviral therapy, antigen and TNF responses persisted and shaped T cell clonal expansion. HIV-1 resided in Th1 polarized, antigen-responding T cells expressing Bcl-2 family anti-apoptotic genes. HIV-1 RNA+ T cell clones were larger in clone size, established during viremia, persistent after viral suppression, and enriched in GZMB+ cytotoxic effector memory Th1 cells. Targeting HIV-1-infected cytotoxic CD4+ T cells and drivers of clonal expansion provides a new direction for HIV-1 eradication.
2022-03-21 | GSE187515 | GEO
Project description:HIV-1 SortSeq identifies HIV-1-infected cells from HIV-1-infected individuals
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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:Investigation of whole genome gene expression level changes in HIV-1 latented infected cells, compared to the replicated cells and control cells.
2012-12-01 | GSE38634 | GEO
Project description:Single-cell multiomics of CD4+ T cell clones in HIV-1 infected individuals
| PRJNA777601 | ENA
Project description:Investigation of whole genome gene expression level changes in HIV-1 latented infected cells, compared to the replicated cells and control cells. In this study, the in vitro steady cell culture was used to explore the mRNA transcription signatures in HIV-1 infection. mRNA profiles were performed and compared among normal control,HIV-1 latency and HIV-1 replication .
2012-12-01 | E-GEOD-38634 | biostudies-arrayexpress