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Metabolic stress is a barrier to Epstein-Barr virus mediated B-cell immortalization

ABSTRACT: Early after infection, Epstein-Barr Virus (EBV) induces a transient period of hyper-proliferation that is suppressed by the activation of the DNA damage response and a G1/S phase growth arrest. This growth arrest prevents long-term outgrowth of the majority of infected cells. We developed a method to isolate and characterize infected cells that arrest after this early burst of proliferation. We used microarray analysis to uncover changes in gene expression that could give us a better understanding of the pathways that attenuate immortalization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76137 | GEO | 2015/12/19

SECONDARY ACCESSION(S): PRJNA306417

REPOSITORIES: GEO

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Metabolic stress is a barrier to Epstein-Barr virus mediated B-cell immortalization

Project description:Early after infection, Epstein-Barr Virus (EBV) induces a transient period of hyper-proliferation that is suppressed by the activation of the DNA damage response and a G1/S phase growth arrest. This growth arrest prevents long-term outgrowth of the majority of infected cells. We developed a method to isolate and characterize infected cells that arrest after this early burst of proliferation. We used microarray analysis to uncover changes in gene expression that could give us a better understanding of the pathways that attenuate immortalization. Human PBMCs were labeled with CellTrace Violet and infected with the B95-8 strain of EBV. At 4 days post-infection, the cells were labeled with a second proliferation dye, CFSE. Cells that proliferated are called PP and those that initially proliferated and then arrested are called PA. Total mRNA was isolated from sorted PA and PP cells using an RNeasy kit . The RNA was processed using an Ambion MessageAmp Premier Package and hybridized to a Human Genome U133 Plus. 2.0 Chip by the Duke Center for Genomic and Computational Biology Microarray Core. The resultant CEL files were RMA normalized (Partek) and the data was analyzed with GenePattern and GSEA v2.

2015-12-19 | E-GEOD-76137 | biostudies-arrayexpress

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Project description:The Epstein-Barr virus nuclear antigen 2 (EBNA2) initiates and maintains the proliferation of infected B cells. In search of additional cellular strategies, that control EBNA2 function, we have performed a label-free mass spectrometry-based quantification of cellular proteins in EBNA2 immuno-precipitates and found polo-like kinase 1 (PLK1) to be bound to EBNA2. EBNA2/PLK1 complex formation is strongly enforced by EBNA2 S379 phosphorylation catalyzed by the mitotic CYCLIN B/CDK1 complex.

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Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells. PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.

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AGS cells infected with Epstein Barr Virus

Project description:Gene expression profile of AGS gastric carcinoma cell line infected in vitro with Epstein-Barr Virus. Some samples also contain are stably transfected with a dominant negative LMP1 construct. 8 total samples. 4 biological replicates of EBV infected cells, 2 biological replicates with EBV infected cells with LMP1DN construct, and 2 biological replicates with EBV infected cells with control vector.

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A Multi-Omics Approach to Epstein-Barr Virus (EBV) Immortalization of B-Cells Reveals Viral-Induced Changes in Chromatin Accessibility and Nucleotide Metabolism

Project description:Epstein-Barr Virus (EBV) immortalizes resting B-lymphocytes through a highly orchestrated process involving extensive reprogramming of host transcription and metabolism. Here, we use multiple omics-based approaches concurrently across the time course of B-cell infection to investigate the underlying mechanisms that control EBV-induced B-cell immortalization. ATAC-seq revealed that over a third of accessible chromatin is altered with the most perturbed sites overlapping Ets-family, including PU.1 and RUNX1 transcription factors. EBV nuclear antigens (EBNAs) clustered with different gene categories and RNA-seq identified the transcriptional response of these gene. Focusing on EBNA1 revealed a selection of gene targets involved in nucleotide metabolism. Metabolomics indicated that adenosine and purine metabolism are significantly altered by EBV immortalization, and we validated that adenosine deaminase (ADA) is a direct and critical target of EBNA1 and the EBV-directed immortalization process. These findings reveal that purine metabolism and ADA inhibitors may be a useful therapeutic for EBV-driven lymphoid cancers

2021-01-15 | GSE155345 | GEO

The Epstein-Barr virus induced tumor suppressor miR-34a is growth promoting in EBV-infected B cells

Project description:Epstein-Barr virus (EBV) infection of primary human B cells drives their indefinite proliferation into lymphoblastoid cell lines (LCLs). B cell immortalization depends on expression of viral latency genes as well as the regulation of host genes. Given the important role of miRNAs in regulating fundamental cellular processes, in this study we assayed changes in host miRNA expression during primary B cell infection by EBV. We observed and validated dynamic changes in several miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced and tumor suppressor miRNAs were largely repressed. However, one miRNA described as a p53-targeted tumor suppressor, miR-34a, was strongly induced by EBV infection and expressed in many EBV and KSHV-infected lymphoma cell lines. The EBV latent membrane protein 1 (LMP1) was sufficient to induce miR-34a requiring downstream NFM-NM-:B activation, but independent of functional p53. Furthermore, over-expression of miR-34a was not toxic in several B lymphoma cell lines and inhibition of miR-34a impaired the growth of EBV transformed cells. This study identifies a pro-growth role for a tumor suppressive miRNA in oncogenic virus-mediated transformation highlighting the importance of studying miRNA function in different cellular contexts. miRNA expression profiling of human B-cells, EBV-infected, proliferating B cells and Monoclonal LCLs from 3 different donors was conducted with the use of up to 2 M-NM-<g total RNA for sample

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The Epstein Barr virus circleRNAome

Project description:The Epstein Barr virus circleRNAome

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The Epstein-Barr virus induced tumor suppressor miR-34a is growth promoting in EBV-infected B cells

Project description:Epstein-Barr virus (EBV) infection of primary human B cells drives their indefinite proliferation into lymphoblastoid cell lines (LCLs). B cell immortalization depends on expression of viral latency genes as well as the regulation of host genes. Given the important role of miRNAs in regulating fundamental cellular processes, in this study we assayed changes in host miRNA expression during primary B cell infection by EBV. We observed and validated dynamic changes in several miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced and tumor suppressor miRNAs were largely repressed. However, one miRNA described as a p53-targeted tumor suppressor, miR-34a, was strongly induced by EBV infection and expressed in many EBV and KSHV-infected lymphoma cell lines. The EBV latent membrane protein 1 (LMP1) was sufficient to induce miR-34a requiring downstream NFκB activation, but independent of functional p53. Furthermore, over-expression of miR-34a was not toxic in several B lymphoma cell lines and inhibition of miR-34a impaired the growth of EBV transformed cells. This study identifies a pro-growth role for a tumor suppressive miRNA in oncogenic virus-mediated transformation highlighting the importance of studying miRNA function in different cellular contexts.

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