Vzv latency
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR832437.fastq.gz | Fastqsanger.gz | |||
| ERR832442.fastq.gz | Fastqsanger.gz | |||
| ERR832443.fastq.gz | Fastqsanger.gz | |||
| ERR832446.fastq.gz | Fastqsanger.gz |
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Project description:Our aim was to investigate the interaction between epidermal differentiation and VZV infection. By means of a calcium-induced keratinocyte differentiation model and RNA-seq we show VZV infection has a profound effect on differentiating keratinocytes and hijacks the normal process of epidermal gene expression to generate a signature resembling patterns of gene expression seen in both heritable and acquired skin-blistering disorders. Analysis of the viral transcriptome provides evidence that VZV replication in skin is tightly linked to differentiation and critically, that late viral gene expression is associated with cellular differentiation. The experiment was performed on human primary keratinocytes under four conditions: undifferentiated/uninfected, uninfected/differentiated, VZV-infected/undifferentiated and VZV-infected/differentiated.
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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 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: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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Project description:RNA profiles of HDF infected with various VZV strains were generated by High-throughput sequencing using Illumina Hi-seq 2500
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