Varicella zoster virus increases lymphocyte adhesion and virus spread through manipulation of IFN-gamma activity
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB61951 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11492545_1.fastq.gz | Fastqsanger.gz | |||
| ERR11492545_2.fastq.gz | Fastqsanger.gz | |||
| ERR11492546_1.fastq.gz | Fastqsanger.gz | |||
| ERR11492546_2.fastq.gz | Fastqsanger.gz | |||
| ERR11492547_1.fastq.gz | Fastqsanger.gz |
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Project description:Varicella-zoster virus (VZV), an alphaherpesvirus, causes chickenpox (varicella) in young children with an annual minimum of 140 million new cases and herpes zoster in senior, a painful and debilitating disease with 3-5‰ incidence. A complex structural transcriptome of VZV, which numerous novel transcripts, transcript isoforms, and unknown splice events are found during cell infection. Circular RNA (circRNA), a newly important component of the transcriptome, is increasing discoveries of circRNA function in mammalian cells. However, VZV encoded circRNA remains unexplored. In this study we demonstration that VZV derived circRNAs are biologically functional and contributed to viral pathogenesis. Using deep RNA-seq following RNase R treatment, we identified and charactered 35, 076 and 54 human and VZV pOka strain circRNAs respectively from VZV infected neuroblastoma cell (SH-SY5Y).
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Project description:Hosts have evolved numerous mechanisms to prevent primary viral infections. Interferon signaling is an important host defense mechanism against primary infection. Interferon gamma (IFN-γ) is a potent cytokine produced following primary varicella-zoster virus (VZV) infection. Furthermore, VZV reactivation correlates with a decline in IFN-γ-producing immune cells. Our previous results showed that pretreatment with 20 ng/ml of IFN-γ completely inhibited VZV replication in lung fibroblast MRC-5 and retinal epithelial ARPE-19, suggesting that IFN-γ-stimulated protein(s) inhibit viral replication. Our microarray analysis revealed that a small subset of interferon-stimulated genes (ISGs) was upregulated by greater than 3.5-fold at 8 h post-treatment in both ARPE-19 and MRC-5 cells compared to those of melanoma MeWo cells. The depletion of IFITM1 and IRF1 by siRNA in IFN-γ-treated cells significantly increased (from 0 to ~1x103 pfu/105 cells) VZV yields. In contrast, the depletion of a nontargeting control (siNTC) did not increase virus yield. Ectopic expression of interferon-induced transmembrane protein 1 (IFITM1) reduced the level of IE62 protein as well as intracellular VZV yield in both ARPE-19 and MeWo cells, but did not reduce the expression level of IE62 mRNA, suggesting that IFITM1 expression reduces the expression level of IE62 by post-transcriptional regulation. IFITM1 also reduced the expression levels of VZV IE62, HSV-1 ICP4, and EHV-1 IEP in ARPE-19 cells
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Project description:Varicella-zoster virus (VZV), an alphaherpesvirus, causes chickenpox (varicella) in young children with an annual minimum of 140 million new cases and herpes zoster in senior, a painful and debilitating disease with 3-5‰ incidence. A complex structural transcriptome of VZV, which numerous novel transcripts, transcript isoforms, and unknown splice events are found during cell infection. Circular RNA (circRNA), a newly important component of the transcriptome, is increasing discoveries of circRNA function in mammalian cells. However, VZV encoded circRNA remains unexplored. The code used in this study and extended data are available from the GitHub repository (https://github.com/ShaominYang/VZV_circRNA)
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Project description:Neuronal reactivation of latent varicella zoster virus (VZV) causes debilitating and protracted pain (post herpetic neuralgia: PHN) in a significant fraction of patients. Productive infection of VZV seems to occur only in humans and primates, so VZV-infected human cells (e.g., MEWO cell line) are used to transmit VZV to rodents. A commonly accepted method of assessing nociception is ipsilateral nocifensive (pain avoidance) behavior in rats which have been injected in a footpad. No such behavioral change is associated with the contralateral (uninjected) footpad. Uninfected MEWO cells or VZV-infected MEWO cells were inoculated into the glabrous region of the right rear footpad of male Sprague-Dawley rats. By 9 days post-inoculation, there was a VZV-dependent decrease in the frequency of neurites that extend from the dermis past the stratum basale layer of the footpad epidermis. Between 7 days and 21 days post-inoculation there was a VZV-dependent increase in nocifensive behaviours in the rats. All VZV-dependent effects occurred in the absence of the productive VZV infection. That is, the virus entered rodent cells and expressed immediate early and early genes, but did not express late genes, synthesize viral DNA, or release infectious virions. Animals which had developed VZV-dependent nocifensive behaviours at 10 days were euthanized, and dorsal root ganglia (L4,5) ipsilateral to inoculation were taken for microarray analysis. Dorsal root ganglia from matching control animals were also analyzed.
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Project description:Neuronal reactivation of latent varicella zoster virus (VZV) causes debilitating and protracted pain (post herpetic neuralgia: PHN) in a significant fraction of patients. Productive infection of VZV seems to occur only in humans and primates, so VZV-infected human cells (e.g., MEWO cell line) are used to transmit VZV to rodents. A commonly accepted method of assessing nociception is ipsilateral nocifensive (pain avoidance) behavior in rats which have been injected in a footpad. No such behavioral change is associated with the contralateral (uninjected) footpad. Uninfected MEWO cells or VZV-infected MEWO cells were inoculated into the glabrous region of the right rear footpad of male Sprague-Dawley rats. By 9 days post-inoculation, there was a VZV-dependent decrease in the frequency of neurites that extend from the dermis past the stratum basale layer of the footpad epidermis. Between 7 days and 21 days post-inoculation there was a VZV-dependent increase in nocifensive behaviours in the rats. All VZV-dependent effects occurred in the absence of the productive VZV infection. That is, the virus entered rodent cells and expressed immediate early and early genes, but did not express late genes, synthesize viral DNA, or release infectious virions. Animals which had developed VZV-dependent nocifensive behaviours at 10 days were euthanized, and dorsal root ganglia (L4,5) ipsilateral to inoculation were taken for microarray analysis. Dorsal root ganglia from matching control animals were also analyzed. Control (uninfected MEWO cells) or VZV-infected MEWO cells were inoculated into the glabrous region of the right rear footpad of male Sprague-Dawley rats. After development of ipsilateral nocifensive behaviour in the VZV-infected animals, the ipsilateral dorsal root ganglia (L4,5) from infected and control animals were taken for microarray analysis.
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Project description:Transcriptome analysis of VZV infected primary human brain vascular adventitial fibroblasts (HBVAFs)
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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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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:Varicella-zoster virus (VZV) encephalitis and meningitis are potential central nervous system (CNS) complications following primary VZV infection or reactivation. With innate immune signalling, and more specifically type I interferon (IFN) signalling, being an important first line cellular defence mechanism against VZV infection, we here investigated the triggering of innate immune responses in a human CNS-like environment. For this, we established and characterised a 5-month matured hiPSC-derived neurospheroid (NSPH) model containing TuJ1+ MAP2+ NeuN+ neurons and GFAP+ S100b+ AQP4+ CD49f+ astrocytes. Immune competence of these NSPHs was demonstrated by secretion of IL-6 and CXCL10 following stimulation with a cocktail of pro-inflammatory stimuli. Subsequently, NSPHs were infected with reporter strains of VZV (eGFP-ORF23 VZV) and Sendai virus (eGFP SeV). Live cell and immunocytochemical analyses demonstrated VZV infection within NSPHs, while SeV infection was limited to the outer NSPH border. Next, a transcript-level immune profiling was performed using NanoString technology to explore innate immune signatures of virus-infected NSPHs. While SeV-infected NSPHs displayed a clear Type I IFN response, in VZV-infected NSPHs no Type I IFN response was activated. Even more, in the latter a strong suppression of genes related to IFN signalling and antigen presentation was noted. Validating these opposite immune signatures in VZV- and SeV-infected NSPHs, cytokine profiling of NSPH supernatant revealed increased secretion of IL6 and CXCL10 by SeV-infected NSPHs, but not by VZV-infected NSPHs. Similarly, immunocytochemical analysis demonstrated upregulation of type I IFN activated anti-viral proteins Mx1, IFIT2 and ISG15 in SeV-infected NSPHs, but not in VZV-infected NSPHs. Furthermore, CD74, a key part of the MHC class II antigen presentation pathway was found to be suppressed in VZV-infected NSPHs. Finally, even though VZV-infection seems to be immunologically ignored in NSPHs, its presence does result in the formation of stress granules throughout the entire NSPH. Concluding, in this study we demonstrate that 5-month matured hiPSC-derived NSPHs display functional innate immune reactivity towards SeV infection, as well as their capability to recapitulate the strong immune evasive behaviour of VZV. Subsequently, this NSPH model has the potential to study viral neuro-immune responses and evasion strategies in a human CNS-like environment.
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