A Variant allele in Varicella-Zoster Virus Glycoprotein B
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45678 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6053180_1.fastq.gz | Fastqsanger.gz | |||
| ERR6053180_2.fastq.gz | Fastqsanger.gz | |||
| ERR6150240_1.fastq.gz | Fastqsanger.gz | |||
| ERR6150240_2.fastq.gz | Fastqsanger.gz | |||
| ERR6150241_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: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.
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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.
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Project description:During primary infection, varicella-zoster virus (VZV) is spread via lymphocytes to skin, where it induces a rash and establishes latency in sensory ganglia. A live, attenuated varicella vaccine (vOka) was generated by using the VZV Oka strain (pOka), but the molecular basis for vOka attenuation remains unknown. Little is known concerning the effects of wild-type or attenuated VZV on cellular gene regulation in the host cells that are critical for pathogenesis. In this study, transcriptional profiles of primary human T cells and fibroblasts infected with VZV in cell culture were determined by using 40,000-spot human cDNA microarrays. Cellular gene transcription in human skin xenografts in SCID mice that were infected with VZV in vivo was also evaluated. The profiles of cellular gene transcripts that were induced or inhibited in infected human foreskin fibroblasts (HFFs), T cells, and skin in response to pOka and vOka infection were similar. However, significant alterations in cellular gene regulation were observed among the three differentiated human cell types that were examined, suggesting specific differences in the biological consequences of VZV infection related to the target cell. Changes in cellular gene transcription detected by microarray analysis were confirmed for selected genes by quantitative real-time reverse transcription-PCR analysis of VZV-infected cells. Interestingly, the transcription of caspase 8 was found to be decreased in infected T cells but not in HFFs or skin, which may signify a tissue-specific antiapoptosis mechanism. The use of microarrays to demonstrate differences in effects on host cell genes in primary, biologically relevant cell types provides background information for experiments to link these various response phenotypes with mechanisms of VZV pathogenesis that are important for the natural course of human infection. A pathogenicity experiment design type is where an infective agent such as a bacterium, virus, protozoan, fungus etc. infects a host organism(s) and the infective agent is assayed. Keywords: pathogenicity_design
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