EBV WGS immunosuppressed
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ABSTRACT:
PROVIDER: PRJEB26469 | ENA |
REPOSITORIES: ENA
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Project description:Whole genome sequencing of EBV from infectious mononucleosis
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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:To investigate the biological differences between EBV-/HIV-, EBV+/HIV- and EBV+/HIV+ classic Hodgkin lymphoma, we performed RNA sequencing of 19 pre-treatment formalin-fixed paraffin-embedded (FFPE) whole lymph node biopsies of cHL.
2025-02-19 | GSE289903 | GEO
Project description:Epstein-Barr virus (EBV) infects over 90% of individuals worldwide and establishes lifelong latency in memory B cells. While this latency is typically controlled by the immune system in healthy people, it can reactivate leading to cell immortalization and post-transplant lymphoproliferative disorders (PTLD), a frequent and potentially life-threatening condition in immunosuppressed patients. Surprisingly, we show that specific antagonists of the histamine H4 receptor (H4R), a G protein-coupled receptor expressed in immune cells, prevent the activation and proliferation of B cells following antigenic-like stimulation (BCR, TLR9, or CD40 ligands) or EBV infection. The lead compound, A943931, inhibited transcriptional but not epigenetic programs associated with B cell activation. Key metabolic genes, were downregulated, with a marked inhibition of glycolysis and oxidative phosphorylation. EBV-driven B cell immortalization was also blocked by H4R antagonists. A943931 similarly impaired energy production in lymphoblastoid cell lines, albeit to a lesser extent than in receptors-stimulated B cells. Finally, A943931 inhibited the growth of the Burkitt lymphoma Daudi xenografted in NSG mice and the development of B cell lymphoma in EBV-infected humanized mice. These findings highlight promising therapeutic potential of some H4R antagonists for EBV-induced lymphoproliferations such as PTLD and, more broadly, for EBV-linked autoimmune disorders.
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Project description:Whole genome sequencing of EBV-transformed B cells in order to determine whether EBV induction of activation-induced cytidine deaminase (AID) produces genome-wide mutations and/or chromosomal rearrangements.
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Project description:We produced and analyzed the transcriptomic profiles of agressive plasmablastic lymphomas to describe their "immune escape" profile, depending on their viral status (HIV, EBV, ...). We used microarrays to compare the global gene expression profile between EBV+ and EBV- PL subtypes. This analysis unveiled the interest of treating EBV+ PL patients by immune checkpoint blockade strategies. Plasmablastic lymphoma (PL) is a subtype of diffuse large B-cell lymphoma occurring frequently in HIV-positive individuals and most often associated with Epstein Barr Virus infection. Despite recent therapeutic progress, PL still is an aggressive lymphoma with adverse prognosis. The aim of this study was to investigate whether the emerging strategies of immune checkpoint blockade could be efficient for PL patients. Here, we produced and analyzed the transcriptomic profiles of such tumors to address this question. Unsupervised hierarchical analysis of PL samples showed that PL segregated according to their EBV-status. Moreover, we report that EBV+ PL displayed a significant association with abundant leucocyte infiltrate and selective T-cell activation signatures, together with high level of inhibitory receptors and immune checkpoint markers. We propose that EBV infection induced an anti-viral cytotoxic immunity which progressively exhausted and promoted the tolerogenic tumor microenvironment of PL. Hence, most EBV+ PL patients presenting an early stage of cancer immune-editing process appear eligible for ICB immunotherapies.
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Project description:Extranodal NK/T-cell, nasal type (hereinafter, nasal T/NK lymphoma), is a distinct clinicopahtologic entity highly associated with EBV. Among nasal T/NK lymphoma, some cases are developed from the long-lasting EBV infection termed chronic active EBV (CAEBV) infection.The clonal expansion of EB infected T- or NK cell are seen in patients with both nasal T/NK lymphoma and CAEBV infection, suggesting that two diseases might partly share the similar mechanism by which EBV affect host cellular genes. Question has thus arisen why a subset of patients with CAEB infection develop into nasal T/NK lymphoma. This study aimed to investigate the virus-host interaction in EBV-associated lymphoma. Keywords = nasak NK/T lymphoma Keywords = chronic active EBV infection Keywords: other
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Project description:We examined the viral epitranscriptome in EBV transformed lymphoblastoid cell lines (LcLs) and EBV-positive Burkitt's lymphoma, Akata cells, using methylated RNA immunoprecipitation followed by sequencing (MeRIP-seq). Biological replicates of ribo-RNA deleted mRNA of each cell type were prepared for MeRIP-seq followed by peak calling using the exome Peak package with settings for stringent peak calling on both strands of the genome.
2023-08-12 | GSE129217 | GEO
Project description:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
Project description:Nasal T/NK lymphoma is a unique subtype of non-Hodgkin lymphoma (NHL) that is aggressive and incurable closely associated with Epstein-Barr virus (EBV)3. The clonal expansion of EB infected T- or NK cell is also seen in patients with chronic active EBV (CAEBV) infection, suggesting that two diseases might partly share a similar mechanism by which EBV affect host cellular genes. In order to understand the pathogenesis of EBV-associated T/NK lymphoproliferative disorders (LPD) and design new therapies, we employed a novel EBV DNA microarray to compare patterns of EBV expression in SNK/T cells established from EBV-associated T/NK LPD. Keywords: parallel sample
2005-09-20 | GSE2414 | GEO