HBVAF cells treated with exosomes from VZV-infected neurons
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851714 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19779993_1.fastq.gz | Fastqsanger.gz | |||
| SRR19779993_2.fastq.gz | Fastqsanger.gz | |||
| SRR19779994_1.fastq.gz | Fastqsanger.gz | |||
| SRR19779994_2.fastq.gz | Fastqsanger.gz | |||
| SRR19779995_1.fastq.gz | Fastqsanger.gz |
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Project description:Exosomes have emerged as essential extracellular signaling vesicles that can deliver proteins and nucleic acids to cells during normal and disease states. Herein, we studied the effects of exosomes produced by VZV-infected human sensory neurons on cerebrovascular cells. Exosomes were isolated from mock- and VZV-infected sensory neurons and protein and nucleic acid was determined by mass spectrometry and Next-Generation Sequencing. Subsequently, mock- and VZV-derived exosomes were applied to primary human brain vascular adventitial fibroblasts (HBVAFs). Overall, exosomes from VZV-infected sensory neurons impacted the pro-inflammatory phenotype of HBVAF cells. The presence of pathogenic exosomes that could circulate throughout the body provides insight into clinical infections.
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Project description:Exosomes from VZV-infected neurons
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Project description:Exosomes have emerged as essential extracellular signaling vesicles that can deliver proteins and nucleic acids to cells during normal and disease states. Herein, we studied the effects of exosomes produced by VZV-infected human sensory neurons on cerebrovascular cells. Exosomes were isolated from mock- and VZV-infected sensory neurons and protein and nucleic acid was determined by mass spectrometry and Next-Generation Sequencing. Subsequently, mock- and VZV-derived exosomes were applied to primary human brain vascular adventitial fibroblasts (HBVAFs). Overall, exosomes from VZV-infected sensory neurons impacted the pro-inflammatory phenotype of HBVAF cells. The presence of pathogenic exosomes that could circulate throughout the body provides insight into clinical infections.
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Project description:Small RNA-seq analysis of exosomes derived from VZV-infected neurons
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Project description:The cellular transcriptomes of VZV-infected fibroblasts and T-lymphocytes have been reported, but not that of human neurons. In order to determine the transcriptional response of human neurons to VZV infection, we generated 95%-pure populations of neurons from hESC, infected them with recombinant GFP-expressing cell-free VZV, and compared their transcriptome to that of human foreskin fibroblasts infected in parallel, using Agilent microarrays. Applying a twofold-change as the cutoff (p-value<0.05), we observed that transcription of 1654 fibroblast and 340 neuronal genes were upregulated, and 955 fibroblast and 38 neuronal genes were downregulated by VZV infection. 223 of these infection-regulated genes were unique to neurons. Gene ontology enrichment analysis revealed several clusters of genes regulated by VZV in neurons and fibroblasts differed. For example, neurons did not show upregulation of innate immune responses, NF-kappaB, response to stress and DNA repair clusters, in contrast to fibroblasts that upregulated these groups. This is the first study of the response of genetically normal human neurons to viral infection. Two-condition experiment, VZV-GFP23- fibroblast cells vs. fibroblast cells, and VZV-GFP23- neuron cells vs. neuron cells. Data from two biological replicates and two technical replicates were used for each condition.
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Project description:The cellular transcriptomes of VZV-infected fibroblasts and T-lymphocytes have been reported, but not that of human neurons. In order to determine the transcriptional response of human neurons to VZV infection, we generated 95%-pure populations of neurons from hESC, infected them with recombinant GFP-expressing cell-free VZV, and compared their transcriptome to that of human foreskin fibroblasts infected in parallel, using Agilent microarrays. Applying a twofold-change as the cutoff (p-value<0.05), we observed that transcription of 1654 fibroblast and 340 neuronal genes were upregulated, and 955 fibroblast and 38 neuronal genes were downregulated by VZV infection. 223 of these infection-regulated genes were unique to neurons. Gene ontology enrichment analysis revealed several clusters of genes regulated by VZV in neurons and fibroblasts differed. For example, neurons did not show upregulation of innate immune responses, NF-kappaB, response to stress and DNA repair clusters, in contrast to fibroblasts that upregulated these groups. This is the first study of the response of genetically normal human neurons to viral infection.
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Project description:The highly conserved herpesvirus glycoprotein complex, gB/gH-gL, mediates membrane fusion during virion entry and cell-cell fusion. Varicella-zoster virus (VZV) characteristically forms multi-nucleated cells, or syncytia, during the infection of human tissues but little is known about this process. The cytoplasmic domain of VZV gB (gBcyt) has been implicated in cell-cell fusion regulation because a gB[Y881F] substitution causes hyperfusion. The gBcyt regulation is necessary for VZV pathogenesis as the hyperfusogenic mutant gB[Y881F] is severely attenuated in human skin xenografts. In this study, gBcyt regulated fusion was investigated by comparing melanoma cells infected with wild type-like VZV or hyperfusogenic mutants. The gB[Y881F] mutant exhibited dramatically accelerated syncytia formation in melanoma cells caused by fusion of infected cells with many uninfected cells, increased cytoskeleton reorganization and rapid displacement of nuclei to dense central structures when compared to pOka using live cell confocal microscopy. VZV and human transcriptomes were concurrently investigated using RNA-seq to identify viral and cellular responses induced when the gBcyt regulation was disrupted by the gB[Y881F] substitution. The expression of four vital VZV genes, ORF61 and glycoproteins, gC, gE and gI, was significantly reduced at 36 hours post infection for the hyperfusogenic mutants. Importantly, hierarchical clustering demonstrated an association of differential gene expression with dysregulated gBcyt-mediated fusion. A subset of Ras GTPase genes linked to membrane remodeling were upregulated in cells infected with the hyperfusogenic mutants. These data implicate the gBcyt in the regulation gB fusion function that, if unmodulated, triggers cellular processes leading to hyperfusion that attenuates VZV infection.
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