Integrative transcriptome analysis of Varicella Zoster Virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB60235 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11179074.fastq.gz | Fastqsanger.gz | |||
| ERR11179077.fastq.gz | Fastqsanger.gz | |||
| ERR11179080.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).
2024-04-27 | GSE223870 | GEO
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)
2024-04-27 | GSE252124 | GEO
Project description:Background : Varicella-zoster virus (VZV), a member of the α-herpesvirus family, is known for causing two distinct diseases: chickenpox (varicella) during the primary infection and shingles (zoster) due to reactivation of the virus later in life. Currently, there were vaccines available to prevent VZV infection, but it is not universally effective, and antiviral treatments for VZV are limited and may come with significant side effects. Thus, development of novel therapeutics is urgently needed. Methods: In the current study, we identified a naturally occurring ALT that inhibits replication of recombinant VZV in human diploid fibroblast (WI-38 cells) and Adult Retinal Pigment Epithelial cell line-19 (ARPE-19 cells) through Western blotting, qPCR and plaque assays. The time-of-addition experiment was carried out to identify the stage at which ALT acted. Meanwhile, the transcriptome was applied for the initial exploration of the mechanism underlying anti-VZV activity. Results : We established a screening model for anti-VZV compounds from which we screened ALT with good antiviral efficacy. Our findings revealed that ALT alleviated cytopathic changes, reduced viral titres, and inhibited the expression of viral genes and proteins in WI-38 cells and ARPE-19 cells. Furthermore, our data showed that ALT inhibits VZV infection at both early and late stages of the viral life cycle. Finally, according to RNA-seq data, multiple inflammatory pathways were involved in this antiviral process, and IL-6 was one of the most critical hub genes. Conclusion : Together, our findings identify ALT as a anti-VZV agent that may prove useful in the treatment of VZV replication.
2025-05-14 | GSE289362 | GEO
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
2021-01-20 | GSE165112 | GEO
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.
2015-03-31 | GSE64345 | GEO
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.
2015-03-31 | E-GEOD-64345 | biostudies-arrayexpress
Project description:Transcriptome analysis of VZV infected primary human brain vascular adventitial fibroblasts (HBVAFs)
2021-11-17 | GSE175797 | GEO
Project description:RNA profiles of HDF infected with various VZV strains were generated by High-throughput sequencing using Illumina Hi-seq 2500
2018-10-18 | GSE121385 | GEO
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.
2014-04-22 | E-GEOD-54385 | biostudies-arrayexpress
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.
2014-04-22 | GSE54385 | GEO