Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Herpes Simplex Virus 1 dramatically alters loading and positioning of RNA Polymerase II on host genes early in infection

ABSTRACT: We used precision nuclear run on (PRO-seq) to determine the location of Pol II at 3 hours post infection with HSV-1 in human epithelial cells. We found HSV-1 decreased Pol II on approxomately 2/3 of cellular genes, but increased Pol II on others. For more than 85% of genes for which transcriptional terminatin could be statistically assed, Pol II was displaced to positions downstream of the normal termination zone suggesting extensive termination defects. Pol II amounts at the promoter, prooter proximal apuse site, and gene bnody were also modulated in a gene-specific manner.

ORGANISM(S): Homo sapiens Drosophila melanogaster

PROVIDER: GSE106126 | GEO | 2018/01/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Herpes Simplex Virus blocks host transcription termination via the bimodal activities of ICP27.

Project description:Infection by viruses, including Herpes Simplex virus-1 (HSV-1), and cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII). The underlying mechanisms, however, remain unclear. Here we demonstrate that, in HSV-1-infected cells, the viral immediate early factor ICP27 is necessary and sufficient for inducing DoTT. Mechanistically, ICP27 directly binds to the essential mRNA 3’ processing factor CPSF, induces the assembly of a dead-end 3’ processing complex, and blocks mRNA cleavage. Remarkably, ICP27 also acts as a sequence-dependent activator of mRNA 3’ processing for HSV-1 and a subset of host genes. Our results suggest that the bimodal activities of ICP27 play a key role in HSV-1-induced host shutoff and that CPSF is a common host factor targeted by multiple viruses. The mechanism described here may have implications for understanding other virus- and cell stress-mediated regulation of transcription termination.

2019-12-15 | GSE128753 | GEO

Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

Project description:Herpes Simplex virus-1 (HSV-1) causes widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) mainly by immediate early gene ICP27. Mechanistically, ICP27 directly binds to the essential mRNA 3’ processingfactor CPSF, induces the assembly of a dead-end 3’ processing complex, and blocks mRNA cleavage. Remarkably, ICP27 also acts as a sequence-dependent activator of mRNA 3’ processing for HSV-1 and a subset of host genes. Our results here show that the bimodal activities of ICP27 play a key role in HSV-1-induced alternative polyadenyalation.

2021-02-26 | GSE151104 | GEO

Herpes Simplex Virus 1 Dramatically Alters Loading and Positioning of RNA Polymerase II on Host Genes Early in Infection.

Project description: Not available

| S-EPMC5874419 | biostudies-literature

ICP22 of Herpes Simplex Virus 1 decreases RNA Polymerase Processivity

Project description:These data files consist of Illumina next seq 500 sequencing data from precision nuclear run-on and global nuclear run-on experiments conducted with human epithelial Hep2 cells that have been infected with human herpes simplex virus-1 (F) strain mutants. The results of these studies suggest that ICP22 is necessary for reducing Pol II processivity on the viral genome which results in its maintenance on the viral genome over the course of infection. While human reads continued to decrease over the time course of infection in the repair virus, this did not occur in the ICP22 deletion virus where over time the number of human reads increased over the time course of infection rather than decreasing. The effects of ICP22 deletion were separable from inhibiting HSV-1 DNA replication to the extent that ICP22 deletion resulted in a decrease in Pol levels only at 6 hpi and not at 3 hpi as was observed in the mutant

2022-01-05 | GSE169574 | GEO

High RNA polymerase II occupancy on herpes simplex virus 1 late genes early in infection suggests progression to elongation is a critical switch to trigger late viral gene expression

Project description:We report the PRO-seq data generated from our analysis of RNA Polymerase II location along the HSV-1 genome at 3 and 6 hpi. This data set includes analysis of the 3hr time point in cells infected in the presence of cycloheximide and the 6hr time point in cells infected in the presence of phosphonoacetic acid, flavopiridol and acyclovir. We have compared the data set to a cytoplasmic mRNA seq data set which is also included. This consisted of polyadenylated, cytoplasmic RNA analyzed at 3 and 6 hpi post infection. Here we are depositing the results from this analysis providing the raw data sequence files along with our bigwig files produced when aligning it to a concatenated genome file containing the drosophila dm3 genome build, the human hg38 genome build, and the included HSV-1 (F-strain) genome with the external repeat sequences deleted. This data provides a nucletide-resolution map of RNA Pol II location in all of the described conditions. By comparing differences between cytoplasmic mRNA production and between Pol II occupancy patterns between samples, we have been able to discern that HSV-1 transcription is a highly regulated process, that involves mechanisms downstream of RNA Pol II recruitment to a HSV-1 promoter region.

2019-12-04 | GSE130342 | GEO

Immediate early proteins of herpes simplex virus transiently repress viral transcription before subsequent activation.

Project description:This study was undertaken to further clarify the roles of HSV-1 immediately early (IE) genes ICP4, ICP0, and ICP22 in early viral transcription. Precision nuclear Run On followed by deep Sequencing (PRO-Seq) was used to identify sites of Pol activity to high resolution on the genomes of HSV-1 viruses bearing mutations in a0, a4 or a22/US1, and corresponding viruses in which these loci were genetically restored. The results indicated that prior to initiating activation of transcription, IE genes first mediate transcriptional repression.

2022-10-18 | GSE202363 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation II

Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.

2017-08-30 | GSE95714 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation I

2017-08-30 | GSE95713 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation III

2017-08-30 | GSE95715 | GEO

Induced pluripotent stem cell derived neuronallineages as human cellular models for Herpes Simplex Virus, type 1 (HSV-1) infections

Project description:Herpes simplex virus type 1 (HSV-1) is a 152 Kb double stranded DNA alpha-herpesvirus, which establishes long life latent infection in sensory neurons. Most of our knowledge regarding HSV-1 latency comes from in vivo studies using small animal models, mainly rodents and rabbits, which are not naturally infected by HSV-1. Furthermore, these animal models do not fully recapitulate the species specific effects of human HSV-1 infection. Human cellular models utilize trigeminal ganglia removed from cadavers or, alternatively, neuron-like cells derived from cancerous cell lines that do not fully reflect effects on normal human neurons. This limitation poses the need to develop an in vitromodel to investigate molecular details of the mechanisms underlying quiescence and reactivation in human neurons. Induced pluripotent stem (iPS) celltechnologies offer an unprecedented opportunity to generate unlimited supplies of neurons and the facility to manipulate such cells in vitro. In this study, we developed an in vitro HSV-1 infection model in human iPS-derived neurons, which displays the main hallmarks of latency defined in animal models and in humans. Our results show for the first time that: i) persistent infection cannot be established in neural progenitor cells (NPCs); ii) the ability of HSV-1 to establish persistent infection is extended to glutamatergic neurons, and not limited to sensory neurons; iii) in neuronal cultures persistently infected with HSV-1, viral genome is localized at the nuclear periphery; iv) HSV-1 acute infection reduces RNA editing at the GluRB site. These results highlight the importance of iPS-based platforms to elucidate unknown aspects of HSV-1 quiescence in human neurons. NPCs were 70-80% confluence

2014-05-02 | E-GEOD-46042 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data