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RNAseq comparison of HSV-1 KOS vs n199 infected cells

ABSTRACT: The abundance of HSV mRNAs was determines over 16h of infection in wt (KOS) and n199 (ICP22 mutant) infected cells. ICP22 is an immediate early gene of HSV that affects gene expression

OTHER RELATED OMICS DATASETS IN: PRJNA430862

ORGANISM(S): Human alphaherpesvirus 1 Homo sapiens

PROVIDER: GSE109420 | GEO | 2018/01/20

REPOSITORIES: GEO

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RNAseq comparison of HSV-1 KOS vs n199 infected cells

Project description:RNAseq comparison of HSV-1 KOS vs n199 infected cells

| PRJNA430862 | ENA

RT-PCR analysis of HSV-1 infected mouse astrocytes and microglia

Project description:Primary mouse microglia and astrocytes were isolated from 6-8 week old C57BL/6J mice and infected with HSV-1 KOS at an MOI of 5 for 12 hours.

2020-07-11 | GSE154176 | GEO

Effect of Cyclohexidmide treatment on early transcription of HSV-1 ΔICP22 and repaired virus

Project description:Study was performed to assess the requirement for HSV-1 IE protein, ICP22, to be expressed to regulate early HSV-1 transcription

2022-10-18 | GSE213098 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)

Project description:Primary human fetal foreskin fibroblasts (HFFF) were infected with the ICP22-null mutant of HSV-1 and HSV-1 Wt strain F at a multiplicity of infection (MOI) of 10 for 8 and 12 hpi. Cells were treated for 8 or 12 hours with the phosphonoacetic acid (PAA) (350ug/ml). Total cellular RNA was isolated using Trizol. T-HF cells were grown either in the presence or absence of DOX. Upon DOX exposure, cells expressed either HA-ICP22 or HA-ICP22 and V5-ICP27. T-HF HA-ICP22 cells were treated with 80 mM KCl (salt stress) for 2 hours before collecting the total RNA. Total cellular RNA was isolated using Trizol.

2023-04-19 | GSE185239 | GEO

Cellular transcriptome upon HSV-1 infection or DUX4 overexpression

Project description:We found that the germline transcription factor double homeobox 4 (DUX4) is upregulated upon infection with wild-type herpes simplex virus-1 (HSV-1). The goal of this experiment was to compare the cellular transcriptome of HEK293T cells that were infected with HSV-1 (KOS strain), or transfected with a plasmid encoding human DUX4.

2018-09-19 | GSE101435 | GEO

Raw RNAseq data of HSV-1-infected mouse skin fibroblasts

Project description:Herpes simplex viruses (HSV) are responsible for a broad variety of human diseases, including cold sores, ocular herpes and herpetic encephalitis, leading to a great burden worldwide. However, the role for sex in herpes infection is controversial and unclear due to the complexity of factors involving in the formation of HSV diseases. Herein, we ask whether there is a sexual dimorphism based on the chromosomal rather than hormonal differences in the primary skin cells during low exposure of HSV. Profiling of male and female transcriptional programs reveals that cytosolic sensing pathway is induced to a greater degree in female cells, correlated with higher yields of infectious virions in male counterparts. Female skin cells distinctively reactivate Xist, a critical component of X inactivation, to silence the expression of the transcriptional repressor on X chromosome, which thereby maintains higher viperin level and further explains the different growth phenotypes between two sexes. Collectively, we propose a model that HSV-1 triggers a sex-specific regulation of antiviral response in the cytosolic sensing signaling via the control of Xist.

2021-12-31 | GSE121651 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq I)

Project description:We report that HSV-1 gives rise to transposase accessible chromatin in gene downstream areas, in regions that show transcription termination defects. We show that the viral protein ICP22 is responsible for this open chromatin.

2023-06-20 | GSE185234 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (Omni-ATAC-seq III)

2023-06-20 | GSE185240 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq II)

Project description:Primary human fetal foreskin fibroblasts (HFFF) were infected with wild-type simplex virus 1 (HSV-1) strain F and null-ICP22 mutant at a multiplicity of infection (MOI) of 10. ATAC-seq libraries were prepared starting with 50,000 cells per condition following the protocol described by Buenrostro et al., Nature Methods 2013

2023-06-20 | GSE185235 | GEO

Parallel G-quadruplexes recruit the HSV-1 transcription factor ICP4 to promote viral transcription in herpes virus-infected human cells

Project description:G-quadruplexes (G4s) are four-stranded nucleic acid structures abundant at gene promoters. They can adopt several distinctive conformations. G4s have been shown to form in the herpes simplex virus-1 (HSV-1) genome during its viral cycle. Here by cross-linking/pull-down assay we identified ICP4, the major HSV-1 transcription factor, as the protein that most efficiently interacts with viral G4s during infection. ICP4 specific and direct binding and unfolding of parallel G4s, including those present in HSV-1 immediate early gene promoters, induced transcription in vitro and in infected cells. This mechanism was also exploited by ICP4 to promote its own transcription. Proximity ligation assay allowed visualization of G4-protein interaction at the single selected G4 in cells. G4 ligands inhibited ICP4 binding to G4s. Our results indicate the existence of a well-defined G4-viral protein network that regulates the productive HSV-1 cycle. They also point to G4s as elements that recruit transcription factors to activate transcription in cells.

2021-09-10 | PXD024743 | Pride

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