Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1033421 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26560311_1.fastq.gz | Fastqsanger.gz | |||
| SRR26560311_2.fastq.gz | Fastqsanger.gz | |||
| SRR26560319_1.fastq.gz | Fastqsanger.gz | |||
| SRR26560319_2.fastq.gz | Fastqsanger.gz | |||
| SRR26560320_1.fastq.gz | Fastqsanger.gz |
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Project description:ABSTRACT: Viral aseptic meningitis is a neuroinflammatory condition that occurs when viruses gain access to the central nervous system (CNS) and induce inflammation. The blood-brain barrier (BBB) is comprised of brain endothelial cells (BECs) that stringently regulate the passage of molecules, toxins, and pathogens from the circulation into the CNS. Through their unique properties, such as complex tight junctions, reduced rates of endocytosis, expression of efflux transporters, and restricted expression of leukocyte adhesion molecules, the BBB is often able to limit pathogen entry into the brain; however, certain neurotropic pathogens, such as coxsackievirus B3 (CVB3) are able to infect the CNS. We have previously demonstrated that CVB3 can infect and disrupt induced pluripotent stem cell-derived brain-like endothelial cells (iBECs), but the host response to this infection remains unknown. Here, we investigate global host transcriptional changes during CVB3 infection of iBECs using RNA sequencing. We validated our data set by exploring pathways altered by CVB3 using quantitative real-time PCR (qPCR) and enzyme-linked immunosorbent assay of upregulated cytokines and interferon signaling molecules. IMPORTANCE: Coxsackievirus B3 (CVB3) is a leading cause of viral aseptic meningitis that can cause severe disease in susceptible individuals. To gain access to the central nervous system, CVB3 must cross central nervous system barriers, such as the blood-brain barrier. Previously, we have shown that CVB3 infects a human stem cell-derived brain-like endothelial cell model. Here, we report the global transcriptome of stem cell-derived brain-like endothelial cells to CVB3 infection and provide proof-of-concept validation of the dataset using molecular biology techniques. These data could inform novel mechanisms of CVB3-mediated blood-brain barrier dysfunction. KEYWORDS: Coxsackievirus B3, blood-brain barrier, brain endothelial cells, RNA sequencing, induced pluripotent stem cells
2024-11-21 | GSE269413 | GEO
Project description:ABSTRACT Background: Viral myocarditis is a life-threatening illness that may lead to heart failure or cardiac arrhythmias. This study examined whether human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics for efficacy. Methods and Results: Human iPSC-CMs were infected with a luciferase-expressing mutant of the coxsackievirus B3 strain (CVB3-Luc). Brightfield microscopy, immunofluorescence, and calcium imaging were used to characterize virally infected hiPSC-CMs. Viral proliferation on hiPSC-CMs was subsequently quantified using bioluminescence imaging. For drug screening, select antiviral compounds including interferon beta 1 (IFNβ1), ribavirin, pyrrolidine dithiocarbamate (PDTC), and fluoxetine were tested for their capacity to abrogate CVB3-Luc proliferation in hiPSC-CMs in vitro. The ability of some of these compounds to reduce CVB3-Luc proliferation in hiPSC-CMs was consistent with the reported drug effects in previous studies. Finally, mechanistic analyses via gene expression profiling of hiPSC-CMs infected with CVB3-Luc revealed an activation of viral RNA and protein clearance pathways within these hiPSC-CMs after IFNβ1 treatment. Conclusions: This study demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to confirm antiviral drug efficacy. Our results suggest that the hiPSC-CM/CVB3-Luc assay is a sensitive platform that could be used to screen novel antiviral therapeutics for their effectiveness in a high-throughput fashion. For this experiment, human induced pluripotent stem cell derived cardiomyocytes were infected with coxsackievirus at multiplicity of infection (MOI) of 5 for 8 hours. Cells were treated with and without interferon beta 1 in order to determine if treatment activates antiviral response genes and/or viral clearance pathways. 4 total samples (2 for each condition) were analyzed
2014-05-19 | E-GEOD-57781 | biostudies-arrayexpress
Project description:We infected two strains of mice, 129S1/SvImJ and 129X1/SvJ, with coxsackievirus type b3 (CVB3) at a dose of 500 pfu/g. 129S1 mice developed increased cardiopathology despite equal viral replication. We hypothesized that the increased cardiopathology might result from an ongoing pathologic host response that we could characterize by global expression profiling. Gene expression was assessed in hearts from 129S1 and 129X1 mice that were uninfected or infected for 6 days. Total RNA obtained from hearts of 3 129S1 and 3 129X1 that were infected or uninfected with CVB3(H3) at 500pfu/g and collected at day 6 post infection
2013-04-01 | E-GEOD-44706 | biostudies-arrayexpress
Project description:ABSTRACT Background: Viral myocarditis is a life-threatening illness that may lead to heart failure or cardiac arrhythmias. This study examined whether human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics for efficacy. Methods and Results: Human iPSC-CMs were infected with a luciferase-expressing mutant of the coxsackievirus B3 strain (CVB3-Luc). Brightfield microscopy, immunofluorescence, and calcium imaging were used to characterize virally infected hiPSC-CMs. Viral proliferation on hiPSC-CMs was subsequently quantified using bioluminescence imaging. For drug screening, select antiviral compounds including interferon beta 1 (IFNβ1), ribavirin, pyrrolidine dithiocarbamate (PDTC), and fluoxetine were tested for their capacity to abrogate CVB3-Luc proliferation in hiPSC-CMs in vitro. The ability of some of these compounds to reduce CVB3-Luc proliferation in hiPSC-CMs was consistent with the reported drug effects in previous studies. Finally, mechanistic analyses via gene expression profiling of hiPSC-CMs infected with CVB3-Luc revealed an activation of viral RNA and protein clearance pathways within these hiPSC-CMs after IFNβ1 treatment. Conclusions: This study demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to confirm antiviral drug efficacy. Our results suggest that the hiPSC-CM/CVB3-Luc assay is a sensitive platform that could be used to screen novel antiviral therapeutics for their effectiveness in a high-throughput fashion. For this experiment, human induced pluripotent stem cell derived cardiomyocytes were infected with coxsackievirus at multiplicity of infection (MOI) of 5 for 8 hours. Cells were treated with and without interferon beta 1 in order to determine if treatment activates antiviral response genes and/or viral clearance pathways.
2014-05-19 | GSE57781 | GEO
Project description:Viruses are obligate intracellular parasites that reshape the ultrastructure, composition and metabolism of host cells to suit their specific needs, although disparate viruses may modify their host in different ways. Such changes may be specifically induced by the virus to support the infection or be part of cellular antiviral responses or stress responses. Here, using state-of-the-art quantitative (phospho)proteomics, we reveal the unique proteome and phosphoproteome dynamics that occur in the host cells infected with the enterovirus coxsackievirus B3 (CVB3).
2020-07-23 | PXD011163 | Pride
Project description:Encoded model contains complete kinetics of infection for coxsackievirus B3 (CVB3), a compact and fast-acting RNA virus. The model consists of separable, detailed modules describing viral binding-delivery, translation-replication, and encapsidation. Specific module activities are dampened by the type I interferon response to viral double-stranded RNAs (dsRNAs), which is itself disrupted by viral proteinases
2021-10-26 | MODEL2110250001 | BioModels
Project description:We infected two strains of mice, 129S1/SvImJ and 129X1/SvJ, with coxsackievirus type b3 (CVB3) at a dose of 500 pfu/g. 129S1 mice developed increased cardiopathology despite equal viral replication. We hypothesized that the increased cardiopathology might result from an ongoing pathologic host response that we could characterize by global expression profiling. Gene expression was assessed in hearts from 129S1 and 129X1 mice that were uninfected or infected for 6 days.
2013-04-01 | GSE44706 | GEO
Project description:The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain. Total RNA obtained from hearts of 3 AJ, 3 B10.A(H2a), 3 CSS3 and 3 B6.chr3AJ that were infected or uninfected with CVB3(CG) at 400pfu/g and collected at day 4 post infection.
2011-05-01 | E-GEOD-19496 | biostudies-arrayexpress
Project description:Male, adolescent A/J mice (4-5 week old) were either infected (IP) with coxsackievirus B3 (CVB3; 105 pfu) or PBS. CVB3 is a cardiotropic virus which leads to cardiac inflammation and fibrosis within 9 days after IP injection. We wanted to know how the virus would impact long term cardiac function, and whether changes in cardiac function could be associated with cardiac transcriptional regulation. At days 3, 9 and 30 days post-infection, hearts were imaged with 2D echocardiography (Sonos 5500, Philips). Briefly, mice were anesthesized subcutaneously with ketamine (0.45mg/kg) and xylazine (0.03mg/kg). Mice were placed in a dorsal recumbency position and the following systolic and diastolic measurements were taken (N=5 heart beats) using an S-12 (12MHz; Sonos 5000, Philips) probe: parasternal long axis, and short axis at the level of the mitral valve and papillary muscles. Measurements were utilized for calculation of wall thickness and functional parameters. Then, heart tissues were flash frozen (N=4 mice/group except CVB3 infected 30 day samples N=2) for hybridization to Affymetrix MG U74Av2 arrays.
2007-09-29 | E-GEOD-1457 | biostudies-arrayexpress
Project description:RNA sequencing of chronic and acute coxsackievirus B3 (CVB3) infection
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