Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide analysis of herpes simplex virus type 1 (HSV-1) infected cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE103763 | GEO | 2017/09/13

SECONDARY ACCESSION(S): PRJNA406943

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression in RAW264.7 cells infected with VSV and HSV-1

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

Gene expression in Src-/- RAW264.7 cells infected with VSV and HSV-1

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

TMEFF1 is a neuron-specific restriction factor for herpes simplex virus

Project description:The brain is highly sensitive to damage caused by infection and inflammation. Herpes simplex virus-1 (HSV-1) is a neurotropic virus and the cause of herpes simplex encephalitis. It is unknown whether neuron-specific antiviral factors control virus replication to prevent infection and excessive inflammatory responses, hence protecting the brain. Using genome-wide CRISPR screening for HSV-1 restriction factors, we identified TMEFF1, which is expressed specifically in CNS neurons and not regulated by type I interferon, as the best-known innate antiviral system controlling virus infections. Depletion of TMEFF1 in stem-cell-derived human neurons led to elevated viral replication and neuronal death upon HSV-1 infection. TMEFF1 blocked the HSV-1 replication cycle at the level of viral entry through interactions with Nectin-1 and non-muscle myosin heavy chain IIA/B, which are core proteins in virus-cell binding and virus-cell fusion, respectively. Importantly, Tmeff1-/- mice exhibited increased susceptibility to HSV-1 infection in the brain but not in the periphery. Within the brain, elevated viral load was observed specifically in neurons. Our study identifies TMEFF1 as a neuron-specific restriction factor essential for prevention of HSV-1 replication in the CNS.

2024-07-24 | GSE268182 | GEO

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody. We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2018-07-07 | GSE116750 | GEO

Genome-wide maps of chromatin state in iBMDM (immortalized bone-marrow-derived macrophages) cells without or with virus infection.

Project description:iBMDM cells were infected with VSV (Vesicular Stomatitis Virus) or HSV-1 (Herpes Simplex Virus 1) for 8 hours, followed by CHIP-seq analysis with H3K27AC antibody (Abcam, ab4729). We find that chromatin state changed with virus infection, some enhacer and superenhancer were induced to promote anti-viral gene expression. Conclusions: virus infection induce enhancer and superenhancer activation.

2022-06-29 | GSE133784 | GEO

RNA-Seq Time-Course Analysis of NPCs Transcriptome in Response to HSV-1 Infection

Project description:The neurogenic niches within the central nervous system serve as essential reservoirs for neural precursor cells (NPCs), playing a crucial role in neurogenesis. However, these NPCs are particularly vulnerable to infection by the herpes simplex virus type 1 (HSV-1). In the present study, we investigated the changes in the transcriptome of NPCs in response to Herpes simplex virus 1 (HSV-1) infection. Using bulk RNA-Seq, the transcriptomes of HSV-1-infected NPCs were compared to those of uninfected samples at different time points in the presence or absence of antivirals.

2024-07-31 | GSE236646 | GEO

RNA polymerase II ChIP-seq in HSV-1 and mock infected cells

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

Understanding Global Changes of the Mouse Brain Proteome after HSV-2 Infection Using a Label-free Shotgun Approach

Project description:Herpes simplex virus type 2 (HSV-2) is a common human pathogen that establishes lifelong latency in neurons of the nervous system. The number of severe central nervous system infections caused by the virus has increased recently. However, the pathogenesis of HSV-2 infection in the nervous system is not fully understood. Here, we demonstrated global proteomic changes in the brain tissue in BALB/c mice vaginally infected with HSV-2.

2022-10-13 | PXD034186 | Pride

Herpes simplex host shutoff attenuates antiviral state

Project description:Herpes simplex virus mutants lacking the vhs gene are severely attenuated in animal models of pathogenesis and exhibit reduced growth in primary cell culture. As a result of these properties vhs-deleted virus have been proposed as live-attenuated viruses. Despite these findings and their implications for vacccines, the mechanisms by which vhs promotes infection in cell culture and in vivo are not understood. In this study we demonstrate that vhs-deficent viruses replicate to reduced levels in interferon(IFN)- primed cells. Furthermore, vhs-defective viruses induce increased levels of IFN? and IFN?-stimulated genes, and increased levels of eIF2? phosphorylation in infected cells. In addition, we demonstrate a generalized over-expression of viral RNAs following infection with a vhs-deficient virus. This suggests increased expression of IFN pathway inducing double stranded RNA, a potent pathogen-associated molecular pattern (PAMP). Together these data show that vhs likely functions to reduce innate immune responses and thereby acts as critical determinant of viral pathogenesis. Keywords: time course, genetic modification Time course (1,3,6,9 & 12h) of HSV infected mouse embryo fibroblasts. Wild type (KOS) virus is co-hybridized with vhs null virus (NHB). Each time-point is hybridized in quadruplicate.

2008-04-03 | E-GEOD-10962 | biostudies-arrayexpress

Identification of viral and host targets of miR-138 by PAR-CLIP analysis of herpes simplex virus 2 infected 293T cells

Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.

2021-11-01 | GSE155402 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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