Mus musculus
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ABSTRACT:
PROVIDER: PRJNA136447 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)
| PRJNA150671 | ENA
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: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: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: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.
2011-05-01 | GSE19496 | GEO
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: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:Fulminant myocarditis (FM) is an acute fatal disease characterised by myocardial inflammation. Our previous study identified soluble growth stimulation- expressed gene 2 (sST2) as a sensitive and specific biomarker for early diagnosis of FM. However, its function in FM remains unclear.In the present study, we observed a marked elevation of sST2 in the plasma and hearts of mice with FM induced by coxsackievirus B3 (CVB3) and explored the main cellular sources of sST2 in FM. Moreover, using recombinant sST2 protein administration and unbiased transcriptomics analyses, we investigated the role and underlying mechanisms of sST2 in FM. Importantly, we found that sST2 has a novel non-classical function in cardiomyocytes, other than acting as an IL-33 decoy receptor. These findings reveal a novel role and action mechanism of sST2 in FM and suggest that sST2 may be a potential therapeutic target for FM.
2024-03-24 | GSE261940 | GEO
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