Null
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB68079 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12245500_1.fastq.gz | Fastqsanger.gz | |||
| ERR12245500_2.fastq.gz | Fastqsanger.gz | |||
| ERR12245501_1.fastq.gz | Fastqsanger.gz | |||
| ERR12245501_2.fastq.gz | Fastqsanger.gz | |||
| ERR12245496_1.fastq.gz | Fastqsanger.gz |
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Project description:HIV-1 infected patients virally suppressed by antiviral treatment harbor a persistent reservoir of replication competent latent HIV-1 infected cells, which constitute the main roadblock to a cure. A main strategy for HIV cure aims to stimulate viral gene expression in latently infected cells so that they can be cleared. Crucial for the design of drugs referred to as “latency-reversing agents” (LRAs) is the identification of molecular targets for latency reversal. The regulatory factors physically associated with and repressing the latent HIV-1 promoter or 5’LTR would provide ideal putative molecular targets for latency reversal. However, due to technical limitations, the comprehensive and unbiased identification of host proteins associated with the latent or active integrated HIV LTR in infected cells not been possible. Here we use dCas9 targeted chromatin and histone enrichment strategy coupled to mass spectrometry (Catchet-MS), to purify the locus-associated dCas9 bait, guided downstream of the HIV-1 transcriptional start site (TSS) in latent and activated HIV-1 infected T cells to identify the 5’LTR bound latent and active regulatory complexes. Catchet-MS identified both previously described as well as novel host factors distinctly associated with the latent versus transcriptionally active HIV-1 5’LTR. Within the identified factors we find the transcription factor IKZF1 to be a novel repressor of the HIV-1 promoter required for maintenance of latency, and thus a molecular target for latency reversal. Finally, we identify the FDA approved drug, Iberdomide, which targets IKZF1 for degradation to be a novel LRA, which reversed latency in latent ex vivo HIV-1 infected primary CD4+ T cells and in cells isolated from HIV-1 infected, aviremic participants.
2022-05-31 | PXD032975 | Pride
Project description:Human immunodeficiency viruses type 1 and 2 (HIV-1 and 2) are known to depend on cellular host machinery for their replication and survival. While most of the studies on cellular proteomic and transcriptomic changes focused on the late-phase of the infection, studies of those changes in the early time-points; especially in the case of HIV-2 infection, are widely lacking. Using 2nd generation HIV-1 and 2 VSV-G pseudotyped lentiviral vectors, we transduced HEK-293T cells, and carried out transcriptomic profiling and proteomic analysis of harvested cells at 2h time point, which is representative of the immediate early-phase events in the infection cycle.
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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.
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Metadata Submitted in BioModels by: Zainab Ashimiyu-Abdusalam
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https://github.com/ersilia-os/eos6hy3
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