Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA214505 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR946043.fastq.gz | Fastqsanger.gz | |||
| SRR946044.fastq.gz | Fastqsanger.gz | |||
| SRR946770.fastq.gz | Fastqsanger.gz | |||
| SRR946771.fastq.gz | Fastqsanger.gz | |||
| SRR946772.fastq.gz | Fastqsanger.gz |
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Project description:The study examined proviral and neighboring gene transcription at sites of intact latent HIV-1 integration in cultured T cells obtained directly from people living with HIV, as well as engineered primary T cells and cell lines and showed that the site of integration has a dominant effect on the transcriptional activity of intact HIV-1 proviruses in the latent reservoir
2024-06-25 | GSE267988 | GEO
Project description:The study examined proviral and neighboring gene transcription at sites of intact latent HIV-1 integration in cultured T cells obtained directly from people living with HIV, as well as engineered primary T cells and cell lines and showed that the site of integration has a dominant effect on the transcriptional activity of intact HIV-1 proviruses in the latent reservoir
2024-06-25 | GSE267987 | GEO
Project description:Targeted HIV cure strategies require definition of the mechanisms that maintain the virus. Here, we tracked HIV replication and the persistence of infected CD4 T cells in individuals with natural virologic control by sequencing viruses, T cell receptor genes, HIV integration sites and cellular transcriptomes. Our results revealed three mechanisms of HIV persistence operating within distinct anatomic and functional compartments. In lymph node, we detected viruses with genetic and transcriptional attributes of active replication in both T follicular helper (TFH) cells and non-TFH memory cells. In blood, we detected inducible proviruses of archival origin among highly differentiated, clonally expanded cells. Linking the lymph node and blood was a small population of circulating cells harboring inducible proviruses of recent origin. Thus, HIV replication in lymphoid tissue, clonal expansion of infected cells, and recirculation of recently infected cells act together to maintain the virus in HIV controllers despite effective antiviral immunity.
2016-07-01 | GSE83482 | GEO
Project description:HIV-1 persists as an integrated DNA provirus in infected cells. Antiretroviral therapy (ART) does not inhibit HIV-1 promoter activity. It is often assumed that HIV-1 reactivation versus latency passively follows host gene activation and repression near the HIV-1 integration site. HIV-1 proviruses integrated into active genes are then transcriptionally active, typically resulting in immune clearance of infected cells. HIV-1 proviruses integrated into repressive chromatin conversely escape immune surveillance. To understand how host gene activity affects HIV-1 transcription, we examined how CRISPR-mediated activation and inhibition of host genes affected HIV-1 nearby chromatin accessibility and RNA transcription using qPCR, ATAC-seq, and strand-specific RNA-seq, in seven Jurkat T cell clones having known HIV-1 integration site. We further examined host CRISPR-mediated HIV-1 activation and inhibition effects on host chromatin accessibility and RNA transcription. We found that host gene activation at the integration site decreased HIV-1 transcription, while host gene inhibition frequently increased HIV-1 transcription. Changes to transcription occurred in both HIV-1 orientations relative to the host gene. Particularly at same-orientation integration sites, reductions in HIV-1 transcription were accompanied by reduced chromatin accessibility at the HIV-1 promoter. However, when HIV-1 integrated in close proximity to host transcription start site, host gene activation increased HIV-1 transcription. When HIV-1 integrated into a non-genic region, we found that HIV-1 increased host chromatin accessibility, remained transcriptionally active, and drove high level of aberrant host RNA transcription. Overall, we found that instead of passively following host gene activity, HIV-1 shapes host chromatin accessibility while an interplay of host factors and transcriptional interference modulate its expression.
2025-10-21 | GSE302221 | GEO
Project description:HIV-1 persists as an integrated DNA provirus in infected cells. Antiretroviral therapy (ART) does not inhibit HIV-1 promoter activity. It is often assumed that HIV-1 reactivation versus latency passively follows host gene activation and repression near the HIV-1 integration site. HIV-1 proviruses integrated into active genes are then transcriptionally active, typically resulting in immune clearance of infected cells. HIV-1 proviruses integrated into repressive chromatin conversely escape immune surveillance. To understand how host gene activity affects HIV-1 transcription, we examined how CRISPR-mediated activation and inhibition of host genes affected HIV-1 nearby chromatin accessibility and RNA transcription using qPCR, ATAC-seq, and strand-specific RNA-seq, in seven Jurkat T cell clones having known HIV-1 integration site. We further examined host CRISPR-mediated HIV-1 activation and inhibition effects on host chromatin accessibility and RNA transcription. We found that host gene activation at the integration site decreased HIV-1 transcription, while host gene inhibition frequently increased HIV-1 transcription. Changes to transcription occurred in both HIV-1 orientations relative to the host gene. Particularly at same-orientation integration sites, reductions in HIV-1 transcription were accompanied by reduced chromatin accessibility at the HIV-1 promoter. However, when HIV-1 integrated in close proximity to host transcription start site, host gene activation increased HIV-1 transcription. When HIV-1 integrated into a non-genic region, we found that HIV-1 increased host chromatin accessibility, remained transcriptionally active, and drove high level of aberrant host RNA transcription. Overall, we found that instead of passively following host gene activity, HIV-1 shapes host chromatin accessibility while an interplay of host factors and transcriptional interference modulate its expression.
2025-10-21 | GSE302199 | GEO
Project description:HIV-1-infected cells that persist despite antiretroviral therapy (ART) are frequently considered ‘‘transcriptionally silent,’’ but active viral gene expression may occur in some cells, challenging the concept of viral latency. Applying an assay for profiling the transcriptional activity and the chromosomal locations of individual proviruses, we describe a global genomic and epigenetic map of transcriptionally active and silent proviral species and evaluate their longitudinal evolution in persons receiving suppressive ART. Using genome-wide epigenetic reference data, we show that proviral transcriptional activity is associated with activating epigenetic chromatin features in linear proximity of integration sites and in their inter- and intrachromosomal contact regions. Transcriptionally active proviruses were actively selected against during prolonged ART; however, this pattern was violated by large clones of virally infected cells that may outcompete negative selection forces through elevated intrinsic proliferative activity. Our results suggest that transcriptionally active proviruses are dynamically evolving under selection pressure by host factors.
2022-01-12 | GSE168337 | GEO
Project description:Targeted HIV cure strategies require definition of the mechanisms that maintain the virus. Here, we tracked HIV replication and the persistence of infected CD4 T cells in individuals with natural virologic control by sequencing viruses, T cell receptor genes, HIV integration sites and cellular transcriptomes. Our results revealed three mechanisms of HIV persistence operating within distinct anatomic and functional compartments. In lymph node, we detected viruses with genetic and transcriptional attributes of active replication in both T follicular helper (TFH) cells and non-TFH memory cells. In blood, we detected inducible proviruses of archival origin among highly differentiated, clonally expanded cells. Linking the lymph node and blood was a small population of circulating cells harboring inducible proviruses of recent origin. Thus, HIV replication in lymphoid tissue, clonal expansion of infected cells, and recirculation of recently infected cells act together to maintain the virus in HIV controllers despite effective antiviral immunity. Fluorescence-activated cell sorting (FACS) was used to sort subsets of CD4 T cells from blood (peripheral blood mononuclear cells; PBMC) and lymph node from a cohort of HIV-infected people with natural control of the virus (termed HIV controllers). Subsets of CD4 T cells that were sorted are as follows: from blood, (1) naïve (N), (2) central memory (CM), (3) transitional memory (TM), and (4) effector memory (EM); from lymph node, (1) naïve (N), (2) non-germinal center T-follicular helpers (nGC), (3) germinal center T-follicular helpers (Tfh), (4) effector memory (EM), and (5) other central memory-like subsets (CMPD1lo57lo, CMPD1lo57hi, and/or CMPD1lo). Total RNA and total DNA were extracted from these sorted subsets in separate fractions using RNAzol RT and DNAzol. Total cellular DNA was used for HIV quantification and sequence analysis as describe in the publication. Total RNA used for mRNA library construction by oligo-dT purification (Dynabeads), random fragmentation by heating in the presence of Magnesium (in form of 5x first-strand buffer, LifeTech), reverse transcription (SuperScript III), and then second-strand synthesis, end repair, a-tailing, and adaptor ligation using NEBNext enzyme master mixes and oligonucleotides. Libraries were sequenced on an Illumina HiSeq2000. Please note that each 'source name' value represent individual who havs HIV infection with natural control of the virus.
2016-07-01 | E-GEOD-83482 | biostudies-arrayexpress
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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