Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356984 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5559322.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to compare small RNA profiles (sRNA-seq) of HSV-1 infected and mock infected human fibroblast KMB17 strain at 48 hours post infection.
2017-08-10 | GSE102470 | GEO
Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.
2012-02-21 | E-GEOD-35943 | biostudies-arrayexpress
Project description:We report transcriptomic data from HSV-1-infected human cells (HFF and MRC5) Herpes simplex virus type I (HSV-1) is a common human pathogen causing cold sores, and in rare cases, severe keratitis and encephalitis. Mouse models are commonly used to study pathogenesis of HSV-1 infection due to the neurotropic properties of HSV make it hard to reach information from infected humans, but mice are not a natural host for this virus. Therefore, it is important to have insights into transcriptional regulation in human cell cultures, which gave us more information before we interpret experimental results from humans and mouse models. Herein, we provide overall transcriptomic data from two HSV-1infected cells, HFF and MRC5. We found that these two human cells downregulated many genes in an antiviral pathway characterized by interferon-stimulated genes.
2021-12-31 | GSE124118 | GEO
Project description:The goal of this study was to determine how RNA poymerase II (Pol II) occupancy changed in response to herpes simplex virus-1 (HSV-1) infection using ChIP-seq of Pol II. ChIP assays were performed 4 hours after cells were infected (or mock infected) with HSV-1. Because host cell Pol II transcribes the HSV-1 genome, the ChIP-seq data also reveal polymerase occupancy on the viral genome.
2015-12-30 | GSE66487 | GEO
Project description:The purpose of this study was to determine which genes are differentially regulated virus infection in RAW264.7 cells. Cells were infected with Vesicular Stomatitis Virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed, focusing on F-box proteins and E3 ubiquitin ligases. RAW264.7 cells were infected with Vesicular Stomatitis Virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.
2016-04-05 | E-GEOD-72077 | biostudies-arrayexpress
Project description:The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.
2016-07-01 | E-GEOD-81675 | biostudies-arrayexpress
Project description:These ChIP-seq analyses identified binding DNAs of ONEUCT2 in Neuro-2a (mouse neuroblastoma)cells. We overexpressed OC2ΔHOX (a gain-of-function mutant) in Neuro-2a cells, and infected the cells with HSV-1 at 40 hours post transfection. Samples infected for 5 hours were sequenced by ChIP for binding DNAs of the OC2 mutant in Neuro-2a cells.
2023-09-18 | GSE241863 | GEO
Project description:The goal of this study was to compare the whole transcriptional profile (RNA-seq) of herpes simplex virus type 1 (HSV-1) infected and mock infected human fibroblast KMB17 strain at 48 hours post infection.There is increasing evidence that circular RNAs (circRNAs) are involved in diverse pathogenesis processes; however, their roles in virus infection remain unclear. Here, we profiled global changes of circRNAs, genes and microRNA (miRNAs) under herpes simplex virus type 1 (HSV-1) infection by RNA-seq. Numerous dysregulated transcripts comprised of 536 circRNAs, 3,885 genes and 207 miRNAs were found during viral infection. The dysregulated genes were enriched to NOD-like receptor signaling pathway, Jak-STAT signaling pathway and pathways of apoptosis, cell cycle progression and cell death, all of which may be implicated in viral pathogenesis and cellular immunity. Further integration analysis of circRNAs, genes and miRNAs reveals putative involvement of circRNAs in viral pathogenesis and antiviral immunity by circRNA-miRNA-gene regulatory axis. This work provides a comprehensive view for dysregulated circRNAs induced by HSV-1 and their interplay with miRNAs and genes, thus offering new insights into the mechanisms of interactions between HSV-1 and its host.
2017-09-13 | GSE103763 | GEO
Project description:B virus and HSV-1 Infected Human Foreskin Fibroblast (HFF) expression profiles
| PRJNA94607 | ENA