T-Cell Responses to Varicella Zoster Virus
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ABSTRACT:
PROVIDER: PRJNA314260 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we screened the differentially expressed genes (DEGs) in SH-SY5Y cells with Varicella-Zoster Virus-Infected using RNAseq technique to explore the molecular mechanisms of Herpes zoster pain
2021-05-12 | GSE141932 | GEO
Project description:quiescent and productive infection of varicella zoster virus in human embryonic stem stem cell-derived neurons
2015-06-22 | E-MTAB-3635 | biostudies-arrayexpress
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: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:Human alphaherpesvirus 3 (Varicella zoster virus) Raw sequence reads
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Project description:<p>Diversity and size of the antigen-specific T cell receptor (TCR) repertoire are two critical determinants for successful control of chronic infection. Varicella zoster virus (VZV) that establishes latency during childhood is able to escape control mechanisms, in particular with increasing age. We examined the TCR diversity of VZV-specific CD4 T cells in individuals older than 50 years by studying three identical twin pairs and three unrelated individuals before and after vaccination with live attenuated VZV. While all individuals had a small number of dominant T cell clones, the breadth of the VZV-specific repertoire differed markedly among different individuals. A genetic influence was seen for the sharing of individual TCR sequences from antigen-specific cells, but not for repertoire richness or the selection of clonal dominance. VZV vaccination favored the expansion of infrequent VZV-specific TCRs including those from naïve T cells while leaving dominant T cell clones mostly unaffected.</p>
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Project description:<p>The study sequenced antibody heavy chain gene rearrangements from 4 identical twin pairs undergoing vaccination with Varicella Zoster viral vaccine.</p>
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Project description:Varicella pneumonia is the most common and severe complication of primary varicella-zoster virus (VZV) infection in adults. Pathogenesis of varicella pneumonia is largely unknown, mainly due to limited availability of clinical specimens and lack of appropriate VZV animal models. Simian varicella virus (SVV) infection of nonhuman primates closely recapitulates clinical and pathogenic features of human VZV disease. This study aimed to elucidate the virus and host factors that contribute to the pathogenesis of varicella pneumonia. The deposited data present changes in gene expression in the lung of SVV-infected cynomolgus macaques (Macaca fascicularis) at 3, 6 and 9 days after infection, and mock-infected control macaques at 3 days after infection.
2020-09-01 | E-MTAB-8485 | biostudies-arrayexpress
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:Interferon-induced transmembrane protein 1 (IFITM1) inhibits Varicella-Zoster Virus Replication
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