EBV WGS infectious mononucleosis
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ABSTRACT:
PROVIDER: PRJEB26470 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Whole genome sequencing of EBV from immunosuppressed patients
| PRJEB26469 | ENA
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.
2023-12-21 | GSE221624 | GEO
Project description:To obtain the site-by-site methylation landscape of the infectious spleen and kidney necrosis virus (ISKNV) genome, whole-genome bisulfite sequencing (WGBS) was performed on an ISKNV strain from 3 duplicate samples.
2023-08-23 | GSE241500 | GEO
Project description:Infection with Epstein-Barr virus (EBV) usually results in asymptomatic infection in the pediatric population. In some pediatric patients, it can lead to infectious mononucleosis (IM) and may be complicated by malignant diseases such as hemophagocytic lymphohistiocytosis (HLH) and chronic active EBV infection (CAEBV). The traditional Chinese medicine (TCM) Sanyang Toujie Decoction (SYTJ) exerts a favorable therapeutic effect on IM associated with EBV infection. However, its active components and underlying mechanisms of action remain unclear. ObjectiveTo clarify the mechanisms of SYTJ against EBV infection in the treatment of pediatric IM by integrating multi-omics and molecular biology approaches. Study DesignWe collected serum samples from healthy children undergoing routine physical examinations, pediatric patients with IM, and pediatric IM patients after SYTJ treatment. An innovative strategy combining proteomics, metabolomics, and molecular biology was adopted to investigate the active components and mechanisms of action of SYTJ. We explored the anti-EBV targets, biological processes, and pathways of SYTJ at the metabolite and protein levels, and established an EBV lytic infection model for validation. ResultsA total of 1,424 chemical components were identified in the fingerprint of SYTJ. Multi-omics and systems biology analyses revealed that the pharmacological mechanisms of SYTJ involve 34 core proteins and 6 core differential metabolites, which are enriched in EBV infection-related key pathways including the Toll-like receptor signaling pathway, glycerophospholipid metabolism, and pentose phosphate pathway. Validation experiments demonstrated that SYTJ could inhibit the proliferation of RAJI and B95-8 cells, promote cell apoptosis, reduce the expression of EBV-EA in RAJI cells and EBV-VCA in B95-8 cells, and suppress EBV-DNA replication. In addition, SYTJ downregulated the mRNA and protein expression of BZLF1 and BMRF1 in B95-8 cells, inhibited EBV lytic replication, upregulated the expression of TOLLIP protein, and suppressed the TLR9/MYD88/NF-κB pathway. ConclusionSYTJ can reduce EBV lytic replication, upregulate TOLLIP protein expression, inhibit the TLR9/MYD88/NF-κB pathway, and alleviate the immune-inflammatory response in the body.
2025-12-07 | PXD071703 |
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: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.
| EGAS00001000955 | EGA
Project description:Epstein-Barr virus (EBV) persistently infects over 90% of the human population and is the causative agent of infectious mononucleosis and human cancers. For the establishment of life-long infection, EBV tampers with the induction of type I interferon (IFN I)-dependent antiviral immunity in the host. How various EBV latency genes help orchestrate this crucial strategy is incompletely defined. Here, we reveal the mechanism by which the EBV nuclear antigen 3A (EBNA3A) inhibits IFNβ induction. Using proximity biotinylation we identify the histone acetyltransferase P300, a member of the IFNβ transcription complex, as a binding partner of EBNA3A. Follow-up experiments further demonstrate that EBNA3A also interacts with the activated IFN-inducing transcription factor IRF3 that collaborates with P300 in the nucleus and both events are mediated by the N-terminal domain of EBNA3A. Mechanistic studies reveal that EBNA3A reduces the binding of IRF3 to the IFNβ promotor, thereby hampering downstream IFN I signaling. These results reveal a novel mechanism by which viral immune evasion takes place.
2025-05-06 | PXD038572 | Pride
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:Epstein-Barr virus (EBV) Rta is a latent-lytic molecular switch evolutionarily conserved in all gamma-herpesviruses. In previous studies, doxycycline-inducible Rta was shown to potently produce an irreversible G1 arrest followed by cellular senescence in 293 cells. Here, we demonstrate that in this system the inducible Rta not only reactivates resident genome of EBV but also that of Kaposi’s sarcoma-associated herpesvirus (KSHV), to similar efficiency. However, Rta-induced senescence program was terminated by the robust viral lytic cycle replication that eventually caused cell death. Furthermore, prior to the abrupt expression of immediate-early protein (EBV BZLF1 or KSHV RTA), Rta simultaneously down-regulates cell cycle activators (c-Myc, CDK6, CCND2) and up-regulates senescence-related genes (p21, 14-3-3s). Since Rta is a viral immediate-early transcriptional activator, it is envisioned that during the initial stage of viral reactivation, Rta may engage to modulate the host transcriptome, to halt cell cycle progression, and to maintain an ideal environment for manufacturing infectious virions. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE24585: Expression profiling of host genes modulated by Epstein-Barr virus (EBV) Rta in HEK293 cells GSE24586: Expression profiling of host genes modulated by Epstein-Barr virus Rta in nasopharyngeal carcinoma cells
2011-03-31 | E-GEOD-24587 | biostudies-arrayexpress
Project description:Epstein-Barr virus (EBV) Rta is a latent-lytic molecular switch evolutionarily conserved in all gamma-herpesviruses. In previous studies, doxycycline-inducible Rta was shown to potently produce an irreversible G1 arrest followed by cellular senescence in 293 cells. Here, we demonstrate that in this system the inducible Rta not only reactivates resident genome of EBV but also that of Kaposi’s sarcoma-associated herpesvirus (KSHV), to similar efficiency. However, Rta-induced senescence program was terminated by the robust viral lytic cycle replication that eventually caused cell death. Furthermore, prior to the abrupt expression of immediate-early protein (EBV BZLF1 or KSHV RTA), Rta simultaneously down-regulates cell cycle activators (c-Myc, CDK6, CCND2) and up-regulates senescence-related genes (p21, 14-3-3s). Since Rta is a viral immediate-early transcriptional activator, it is envisioned that during the initial stage of viral reactivation, Rta may engage to modulate the host transcriptome, to halt cell cycle progression, and to maintain an ideal environment for manufacturing infectious virions. This SuperSeries is composed of the SubSeries listed below.
2011-03-31 | GSE24587 | GEO