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ABSTRACT:
PROVIDER: PRJEB86994 | ENA |
REPOSITORIES: ENA
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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:The alphaherpesvirus Varicella-Zoster Virus (VZV) infects most humans. It causes chickenpox, shingles and rare severe central nervous system (CNS) pathologies. To gain molecular insights in the virus’ pathobiology, we conducted a proteomic survey on the interactions and effects of 64 VZV proteins, and VZV infection-induced perturbations, in neuronal SK-N-BE2 cells. This identified 900 interactors and 3618 regulated host proteins (https://varizonet.innatelab.org). Data integration and functional validations of the identified host proteins unveiled NPHP4 as VZV restriction factor. Combining whole exome of patients with VZV-associated CNS pathologies identified the NPHP4 S862N variant. Importantly, the S862N mutation impaired NPHP4's antiviral activity, and supressed its interactions with 14-3-3 proteins, as measured by affinity-purification.
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Project description:The alpha-herpesvirus Varicella-Zoster Virus (VZV), the causative agent of chicken pox, infects most humans worldwide and remains latent in peripheral neuronal cells for life. Its reactivation triggers herpes zoster and sporadic disseminated infection, in particular in the central nervous system (CNS) where it is associated with severe pathologies. VZV replication is efficiently controlled with antivirals, however the emergence of treatment-resistant VZV variants constitutes an increasing healthcare issue, calling for in-depth analysis of molecular VZV-host interactions to foster general knowledge and promote identification of novel therapeutic targets. Here we conducted a mass spectrometry-based survey in neuronal SK-N-BE2 cells, combining proteome analysis of VZV-infected cells with systematic characterization of VZV proteins’ functions through identifying their individual host partners and effects on the host proteome. To generate this specific dataset, we used AP-MS and a Bayesian modelling approach to characterize the VZV-host interactome. We collectively identified 1184 interactions between 56 viral and 900 human proteins.
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Project description:The alpha-herpesvirus Varicella-Zoster Virus (VZV), the causative agent of chicken pox, infects most humans worldwide and remains latent in peripheral neuronal cells for life. Its reactivation triggers herpes zoster and sporadic disseminated infection, in particular in the central nervous system (CNS) where it is associated with severe pathologies. VZV replication is efficiently controlled with antivirals, however the emergence of treatment-resistant VZV variants constitutes an increasing healthcare issue, calling for in-depth analysis of molecular VZV-host interactions to foster general knowledge and promote identification of novel therapeutic targets. Here we conducted a mass spectrometry-based survey in neuronal SK-N-BE2 cells, combining proteome analysis of VZV-infected cells with systematic characterization of VZV proteins’ functions through identifying their individual host partners and effects on the host proteome. In this dataset, we systematically assessed proteome changes elicited by the expression of individual viral proteins – the so called “effectome”, which allowed us to gain unprecedented insights in the activity of individual VZV ORFs.
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Project description:The alpha-herpesvirus Varicella-Zoster Virus (VZV), the causative agent of chicken pox, infects most humans worldwide and remains latent in peripheral neuronal cells for life. Its reactivation triggers herpes zoster and sporadic disseminated infection, in particular in the central nervous system (CNS) where it is associated with severe pathologies. VZV replication is efficiently controlled with antivirals, however the emergence of treatment-resistant VZV variants constitutes an increasing healthcare issue, calling for in-depth analysis of molecular VZV-host interactions to foster general knowledge and promote identification of novel therapeutic targets. Here we conducted a mass spectrometry-based survey in neuronal SK-N-BE2 cells, combining proteome analysis of VZV-infected cells with systematic characterization of VZV proteins’ functions through identifying their individual host partners and effects on the host proteome. We functionally evaluated the 116 most prominent host proteins by loss-of-function assay and unveiled yet uncharacterized dependency and restriction factors. In particular, the transcriptional regulators MPP8 and ZNF280D, interactors of VZV ORFs 4 and 12, and ORF63, respectively, were critical for VZV spread, thus highlighting these viral-host protein interactions as strategic targets to limit infection.
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Project description:The alpha-herpesvirus Varicella-Zoster Virus (VZV), the causative agent of chicken pox, infects most humans worldwide and remains latent in peripheral neuronal cells for life. Its reactivation triggers herpes zoster and sporadic disseminated infection, in particular in the central nervous system (CNS) where it is associated with severe pathologies. VZV replication is efficiently controlled with antivirals, however the emergence of treatment-resistant VZV variants constitutes an increasing healthcare issue, calling for in-depth analysis of molecular VZV-host interactions to foster general knowledge and promote identification of novel therapeutic targets. Here we conducted a mass spectrometry-based survey in neuronal SK-N-BE2 cells, combining proteome analysis of VZV-infected cells with systematic characterization of VZV proteins’ functions through identifying their individual host partners and effects on the host proteome. We identified host proteins and signalling routes involved in VZV-mediated cell cycle progression, blockade of apoptosis, alteration of neuronal differentiation and innate immunity evasion. We functionally evaluated the 116 most prominent host proteins by loss-of-function assay and unveiled yet uncharacterized dependency and restriction factors. We generated stable knockout BFP positive SK-N-BE2 cells to validate their function in VZV replication assays as compared to Non-Targeting-Control (NTC) 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. 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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