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Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells

ABSTRACT: Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells

PROVIDER: PRJNA915089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22870349.fastq.gz	Fastqsanger.gz
	SRR22870350.fastq.gz	Fastqsanger.gz
	SRR22870351.fastq.gz	Fastqsanger.gz
	SRR22870352.fastq.gz	Fastqsanger.gz
	SRR22870353.fastq.gz	Fastqsanger.gz

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Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells [EBV WGS]

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Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells [RNA-Seq]

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Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells [RNA-Seq]

Project description:Epidemiological studies have demonstrated that Epstein-Barr virus (EBV) is a known etiologic risk factor, and perhaps prerequisite, for the development of MS. EBV establishes life-long latent infection in a subpopulation of memory B cells. Although the role of memory B cells in the pathobiology of MS is well established, studies characterizing EBV-associated mechanisms of B cell inflammation and disease pathogenesis in EBV (+) B cells from MS patients are limited. Accordingly, we analyzed spontaneous lymphoblastoid cell lines (SLCLs) from multiple sclerosis patients and healthy controls to study host-virus interactions in B cells, in the context of an individual’s endogenous EBV. We identify differences in EBV gene expression and regulation of both viral and cellular genes in SLCLs. Our data suggest that EBV latency is dysregulated in MS SLCLs with increased lytic gene expression observed in MS patient B cells, especially those generated from samples obtained during “active” disease. Moreover, we show increased inflammatory gene expression and cytokine production in MS patient SLCLs and demonstrate that tenofovir alafenamide, an antiviral that targets EBV replication, decreases EBV viral loads, EBV lytic gene expression, and EBV-mediated inflammation in both SLCLs and in a mixed lymphocyte assay. Collectively, these data suggest that dysregulation of EBV latency in MS drives a pro-inflammatory, pathogenic phenotype in memory B cells and that this response can be attenuated by suppressing EBV lytic activation. This study provides further support for the development of antiviral agents that target EBV-infection for use in MS.

2023-12-21 | GSE221623 | GEO

Unstable EBV latency drives inflammation in multiple sclerosis patient derived spontaneous B cells [EBV WGS]

Project description:Epstein-Barr virus (EBV) is an etiologic risk factor, and likely prerequisite, for the development of multiple sclerosis (MS). However, the role of EBV infected B cells in the immunopathology of MS is not well understood. Here, we characterized spontaneous lymphoblastoid cell lines (SLCLs) isolated from MS patients and healthy controls (HC) ex vivo to study EBV and host gene expression in the context of an individual’s endogenous EBV. SLCLs derived from MS patient B cells during active disease had higher EBV lytic gene expression than SLCLs from MS patients with stable disease or HCs. Host gene expression analysis revealed activation of pathways associated with hypercytokinemia and interferon signaling in MS SLCLs and differential expression of several genes, including upregulation of forkhead box protein 1 (FOXP1), which contributes to EBV lytic gene expression. In addition, we demonstrate that antiviral approaches targeting EBV replication decreased inflammatory cytokine production and diminished autologous CD4+ T cell responses. These data suggest that dysregulation of intrinsic B-cell control of EBV gene expression drives a pro-inflammatory, pathogenic B cell phenotype that can be attenuated by suppressing EBV lytic gene expression.

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Project description:Epidemiological studies have demonstrated that Epstein-Barr virus (EBV) is an etiologic risk factor, and perhaps prerequisite, for the development of MS. EBV establishes life-long latent infection in a subpopulation of memory B cells. Although B cells play a key role in the pathobiology of MS, EBV-associated mechanisms of B cell inflammation and disease pathogenesis in EBV (+) B cells from MS patients are not well characterized. Accordingly, we obtained lymphoblastoid lines (LCLs) and spontaneous LCLs (SLCLs), distinguished by their transformation with lab strain (B95.8) or endogenous EBV, respectively, from MS patients and healthy controls to study host-virus interactions in B cells. Here, we use transcriptomics and genomics-based approaches to identify differences in EBV gene expression and regulation of both viral and cellular genes in LCLs compared to SLCLs and between SLCLs generated from healthy controls and MS patients during “active” or “stable” periods of disease activity. We demonstrate increased lytic gene expression in SLCLs derived from MS patient B cells, especially those generated from peripheral blood mononuclear cells (PBMCs) obtained during “active” disease.

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