Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1065137 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27560600_1.fastq.gz | Fastqsanger.gz | |||
| SRR27560600_2.fastq.gz | Fastqsanger.gz | |||
| SRR27560601_1.fastq.gz | Fastqsanger.gz | |||
| SRR27560601_2.fastq.gz | Fastqsanger.gz | |||
| SRR27560602_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Tissue resident memory T cells (TRM) provide superior protection against infection localised to extra-lymphoid compartments in the body. Here we show that CD103+CD8+ TRM cells develop in skin from killer cell lectin-like receptor (KLR)G1-negative precursors that selectively infiltrate the epithelial layer. In the skin, a combination of chemokine-guided epithelial entry, local interleukin (IL)-15 and transforming growth factor (TGF)-β signalling is required for formation and survival of these long-lived memory cells. Importantly, TRM differentiation results in the gradual acquisition of a unique transcriptional profile that differs from that expressed by memory cells in the circulation and other types of skin-resident intra-epithelial T cells, such as the dendritic epidermal T cells (DETC). We provide a comprehensive molecular and developmental framework for the local differentiation of a distinct type of peripheral memory T cell that contributes to an important first-line of immune defence in barrier tissues such as skin and mucosa. 24 samples were analyzed: 3 replicates of memory gB-T CD8+. CD103+ T cells isolated from the skin of C57/BL6 mice on day 30 p.i. with HSV KOS. 3 replicates of memory P14 CD8+ T cells isolated from gut of mice on day 60 p.i. with LCMV Armstrong. 3 replicates of memory gB-T CD8+ T cells from the lung of mice on day 30 p.i. with influenza WSN. 3 replicates of memory CD62L high CD8+ T cells from the spleen of mice on day 30 p.i. with HSV KOS. 3 replicates of memory CD62L low CD8+ T cells from the spleen of mice of day 30 p.i. with HSV KOS. 3 replicates of γδ-DETC isolated from the skin of C57/BL6 mice on day 30 p.i. with HSV KOS. 3 replicates of αβ-DETC from naive TCRδ-/- mice; and 3 replicates of naive gB-T CD8+ T cells from the spleen of naive gB-T transgenic mice.
2013-10-01 | E-GEOD-47045 | biostudies-arrayexpress
Project description: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
2018-01-20 | GSE109420 | GEO
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
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:Protein palmitoylation regulates diverse aspects of cellular function and organization and plays a key role in host immune responses to infection. Palmitoylation also modulates the function and localization of virus-encoded proteins. In Serwa et al. (doi:10.1016/j.chembiol.2015.06.024), we employed chemical proteomics tools, bio-orthogonal palmitic acid analogue (heptadec-16-ynoic acid, YnPal), and a multi-functional capture reagent (AzTB) to study palmitoylation events during infection with three strains of herpes simplex virus (HSV-1[17], HSV-1[KOS], HSV-2[186]). We found that a significant fraction of the viral proteome (twelve HSV-encoded proteins) undergoes palmitoylation; we identified a number of virus membrane glycoproteins, structural proteins, and kinases. Furthermore, we identified palmitoylation sites on five HSV-encoded proteins utilising a complementary methodology (Acyl-RAC). This paper also reports selective HSV-induced alterations to palmitoylation and myristoylation of host proteins.
2022-03-02 | PXD002708 | Pride
Project description:PURPOSE: Acyclovir (ACV) is an effective antiviral agent for treating lytic Herpes Simplex virus, type 1 (HSV-1) infections, and it has dramatically reduced the mortality rate of herpes simplex encephalitis. However, HSV-1 resistance to ACV and its derivatives is being increasingly documented, particularly among immunocompromised individuals. The burgeoning drug resistance compels the search for a new generation of more efficacious anti-herpetic drugs. We have previously shown that 3-epi-trans-dihydrolycoricidine (R430), a lycorane-type alkaloid derivative, effectively inhibits HSV-1 infections in cultured cells. METHODS: We employed human induced pluripotent stem cells-derived neurons (hiPSC-neurons) and neural progenitor cells (hiPSC-NPCs) to investigate the antiviral activity of R430 on HSV-1 and Zika (Strain XX), respectively. hiPSC line 73-56010-02 employed in this study established at the National Institute of Mental Health (NIMH) Center for Collaborative Studies of Mental Disorders-funded Rutgers University Cell and DNA Repository (http://www.rucdr.org/mental-health) (RUCDR). hiPSC- neurons and hiPSC-NPCs were generated as previously described (D’Aiuto et al. Organogenesis. 2014;10(4):365-77). hiPSC based assays for HSV-1 infection. We used a genetically engineered HSV-1 KOS strain that expresses enhanced green fluorescent protein (EGFP) and red fluorescent protein (RFP) under the control of immediate early and late gene promoters, respectively (33). To determine the optimal conditions for evaluating drug effects, hiPSC-neurons cells were infected for 2 hours (multiplicity of infection, MOI=0.3), after which the inocula were replaced with media containing R430 (10 µM) or vehicle (DMSO). Separately, cells were incubated in media containing R430 (10 µM) or vehicle in the absence of HSV-1. All assays were conducted in triplicate. Cells were harvested after 6 hours post infection (hpi), 12 hpi, or 24 hpi, DNA was extracted using (QIAamp DNA Mini Kit, (Qiagen) and DNA conentrations were estimated. Subsequently, the EGFP locus was amplified to estimate viral copy number using custom primers (34). A significant increase in viral copy number was noted in vehicle treated cells after 12h and 24h, but not after 6h. Substantial reduction in viral copy number was found following incubation with R430 at 12h or 24h. The 12h incubation period was therefore selected for subsequent studies examining gene expression (see below).
2018-11-19 | GSE111656 | 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.
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Project description:In this study, we investigated the effects of HSV-1 infection on tau phosphorylation in human brain cortical organoids. Our findings demonstrate that HSV-1 triggers nuclear accumulation of phosphorylated tau in neurons within the developing cortical plate as well as in neural precursor cells (NPCs) in the ventricular/subventricular-like zones of these differentiating cortical structures. Antiviral treatment effectively inhibited nuclear tau accumulation in both KOS- and 17syn+-infected organoids. Importantly, for the first time we provide evidence of a potential interaction of phosphorylated tau with HSV-1 genome. Furthermore, we ruled out the involvement of the Cyclin-dependent kinase 5 (Cdk5) in the nuclear phosphorylation of tau. Finally, we show that HSV-1 causes a significant alteration in the abundance of components of nuclear speckles and proteins known to be associated with neurodegenerative diseases.
2025-05-06 | PXD047281 | Pride