Human gammaherpesvirus 4
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA172189 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR534597.fastq.gz | Fastqsanger.gz | |||
| SRR534598.fastq.gz | Fastqsanger.gz | |||
| SRR534599.fastq.gz | Fastqsanger.gz | |||
| SRR534600.fastq.gz | Fastqsanger.gz | |||
| SRR534601.fastq.gz | Fastqsanger.gz |
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Project description:Expression of EBV miRNAs in numerous EBV-positive cell lines
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Project description:We used Precision Nuclear Run-on followed by Deep Sequencing (PRO-Seq) to investigate RNA Polymerase (Pol) activity during Epstein-Barr Virus (EBV) reactivation in EBV positive Burkitt's lymphoma cell lines Mutu-I and Akata. Nuclei were harvested from latent cells and after treatment with NaB/TPA (Mutu-I) or anti-IgG (akata) to stimulate reactivation at 1 and 4 and 12h. We identified multiple sites on the EBV genome enriched with Pol displaying distinct patterns of activity, which showed an association with CTCF and open chromatin.
2023-01-06 | GSE188584 | GEO
Project description:Epstein-Barr virus (EBV) is a ubiquitous gammaherpes virus that establishes a life-long latency in over 90% of the world's population. Epstein Barr Nuclear Antigen 1, EBNA1, is the only viral protein consistently detected in all viral latency programs, as well as in all forms of EBV-associated malignancies. EBNA1 plays critical roles in the viral life cycle by fostering the replication and maintenance of the extrachromosomal viral genome as well as enhancing transcription from multiple viral promoters. Using chromatin immunoprecipitation and human promoter microarrays (an analysis termed ChIP-chip) we found that EBNA1 binds site specifically within multiple human promoters. To determine whether EBNA1â??s binding to these promoters perturbed gene expression, we measured the levels of cellular mRNAs by microarrays when EBNA1 was inhibited by a dominant negative derivative of EBNA1 (DomNeg1). Keywords: viral regulation of cellular genes We analysed mRNA expression from the EBV-positive lymphoblastoid cell line 721 transduced with either a control (empty) retroviral vector or a DomNeg1-encoding retroviral vector. For ChIP-chip, DNA from immunoprecipitated chromatin using a anti-EBNA1 antibody (IH4) along with total chromatin was hybridized to a Nimblegen human promoter arrays (CHAR0150-HP2). A single ChIP-chip experiment was performed with DNAs pooled equally from three independent ChIP experiments.
2010-05-14 | E-GEOD-13315 | biostudies-arrayexpress
Project description:Epstein-Barr Virus (EBV), which is associated with multiple human tumors, persists as a minichromosome in the nucleus of B-lymphocytes and induces malignancies through incompletely understood mechanisms. Here, we present a large-scale functional genomic analysis of EBV. Our experimentally generated nucleosome positioning maps and viral protein binding data were integrated with over 700 publicly available high-throughput sequencing data sets for human lymphoblastoid cell lines mapped to the EBV genome. We found that viral lytic genes are coexpressed with cellular cancer-associated pathways, suggesting that the lytic cycle may play an unexpected role in virus-mediated oncogenesis. Host regulators of viral oncogene expression and chromosome structure were identified and validated, revealing a role for the B-cell-specific protein Pax5 in viral gene regulation and the cohesin complex in regulating higher order chromatin structure. Our findings provide a deeper understanding of latent viral persistence in oncogenesis and establish a valuable viral genomics resource for future exploration. Six sequencing experiments were performed. One EBNA1 ChIP-seq was controlled with IgG ChIP-seq. Two MNase-seq biological replicates were each conrolled by input seq using the same cells subjected to MNase digestion.
2012-08-28 | E-GEOD-39913 | biostudies-arrayexpress
Project description:The Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1) protein is required for the establishment of EBV latent infection in proliferating B-lymphocytes. EBNA1 is a multifunctional DNA-binding protein that stimulates DNA replication at the viral origin of plasmid replication (OriP), regulates transcription of viral and cellular genes, and tethers the viral episome to the cellular chromosome. EBNA1 also provides a survival function to B-lymphocytes, potentially through its ability to alter cellular gene expression. Chromatin-immunoprecipitation (ChIP) combined with massively parallel deep-sequencing (ChIP-Seq) was used to identify cellular sites bound by EBNA1. Sites identified by ChIP-Seq were validated by conventional real-time PCR, and ChIP-Seq provided quantitative, high-resolution detection of the known EBNA1 binding sites on the EBV genome at OriP and Qp. We identified at least one cluster of unusually high-affinity EBNA1 binding sites on chromosome 11, between the divergent FAM55D and FAM55B genes. A consensus for all cellular EBNA1 binding sites is distinct from those derived from the known viral binding sites, suggesting that some of these sites are indirectly bound by EBNA1. We conclude that EBNA1 can interact with a large number of cellular genes and chromosomal loci in latently infected cells, but that these sites are likely to represent a complex ensemble of direct and indirect EBNA1 binding sites. Study of Epstein-Barr virus (EBV)
2011-07-16 | E-GEOD-30709 | biostudies-arrayexpress
Project description:Chromatin structure plays a central role in the regulation of Epstein-Barr Virus (EBV) latency. The histone variant H2A.Z.1 has been implicated in chromatin structures associated with initiation of transcription and DNA replication. Here, we examined the role of H2AZ.1 in the regulation of EBV chromatin and gene expression during EBV latent infection in two different EBV cancer cell models. We found that H2A.Z.1 is highly enriched with EBNA1 binding sites at oriP and Qp, and to a lesser extent with transcriptionally active CTCF binding sites on the EBV genomes in both Mutu I Burkitt lymphoma (BL) and SNU7-19 EBV-associated gastric carcinoma (EBVaGC) cell lines. RNA-interference depletion of H2A.Z.1 resulted in the reactivation of viral lytic genes (ZTA and EAD) and increases viral DNA copy numbers in both MutuI and SNU719 cells. H2A.Z depletion also led to a decrease in EBNA1 binding to oriP and Qp, on the viral episome as well as on plasmids independently of other viral genes and genomes. H2A.Z.1 depletion also reduced peaks of H3K27ac and H4K20me3 at regulatory elements in the EBV genome. In the cellular genome, H2A.Z.1 colocalized with only a subset of EBNA1 binding sites and H2A.Z.1 depletion altered transcription of genes associated with myc targets and mTORC1 signaling. Taken together, these findings indicate that H2A.Z.1 plays an important regulatory role in the regulation of EBNA1 chromatin binding and function in the EBV episome and host chromosome, as well as the epigenetic programming of the latent episome.
2026-02-13 | GSE289711 | GEO
Project description:Chromatin structure plays a central role in the regulation of Epstein-Barr Virus (EBV) latency. The histone variant H2A.Z.1 has been implicated in chromatin structures associated with initiation of transcription and DNA replication. Here, we examined the role of H2AZ.1 in the regulation of EBV chromatin and gene expression during EBV latent infection in two different EBV cancer cell models. We found that H2A.Z.1 is highly enriched with EBNA1 binding sites at oriP and Qp, and to a lesser extent with transcriptionally active CTCF binding sites on the EBV genomes in both Mutu I Burkitt lymphoma (BL) and SNU7-19 EBV-associated gastric carcinoma (EBVaGC) cell lines. RNA-interference depletion of H2A.Z.1 resulted in the reactivation of viral lytic genes (ZTA and EAD) and increases viral DNA copy numbers in both MutuI and SNU719 cells. H2A.Z depletion also led to a decrease in EBNA1 binding to oriP and Qp, on the viral episome as well as on plasmids independently of other viral genes and genomes. H2A.Z.1 depletion also reduced peaks of H3K27ac and H4K20me3 at regulatory elements in the EBV genome. In the cellular genome, H2A.Z.1 colocalized with only a subset of EBNA1 binding sites and H2A.Z.1 depletion altered transcription of genes associated with myc targets and mTORC1 signaling. Taken together, these findings indicate that H2A.Z.1 plays an important regulatory role in the regulation of EBNA1 chromatin binding and function in the EBV episome and host chromosome, as well as the epigenetic programming of the latent episome.
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Project description:The viral nuclear antigen 1 (EBNA1) of Epstein Barr (EBV) features two functionally redundant Arginine-Glycine (RG) repeats that contain symmetrically and asymmetrically di-methylated (SDMA/ADMA) and also mono-methylated (MMA) Arginine residues. We generated mouse monoclonal antibodies against the mono-methylated RG-repeat between aa 328-377. In addition to detect MMA-EBNA1, we aimed at the identification of cellular proteins that are bound to MMA-modified EBNA1 in EBV-positive Raji cells.
2025-03-05 | PXD051181 | Pride
Project description:The Epstein-Barr virus (EBV) is associated with lymphoid and epithelial cancers. Initial EBV infection alters lymphocyte gene expression, inducing cellular proliferation and differentiation as the virus transitions through consecutive latency transcription programs. Cellular microRNAs (miRNAs) are important regulators of signaling pathways and are implicated in carcinogenesis. The extent to which EBV exploits cellular miRNAs is unknown. Using micro-array analysis and quantitative PCR, we demonstrate differential expression of cellular miRNAs in type III versus type I EBV latency including elevated expression of miR-21, miR-23a, miR-24, miR-27a, miR-34a, miR-146a and b, and miR-155. In contrast, miR-28 expression was found to be lower in type III latency. The EBV-mediated regulation of cellular miRNAs may contribute to EBV signaling and associated cancers. There were two major objectives for this study. The first objective was to determine whether EBV infected cells exhibiting type I latency influence cellular microRNA expression. For this study, four EBV negative derivatives of the type I latency cell line, Mutu I, were derived by retroviral infection with a dominant negative from of the EBV episomal replication factor, EBNA1. RNA from these four clones were compared to parental EBV positive Mutu I cells. Four dual labeling experiments were carried out for this comparison with dye reversal for every second pair of RNAs. The second objective was to determine whether EBV type III latency cells exhibit altered cellular microRNA gene expression compared to type I latency cells or EBV negative B cells. Four dual labeling experiments were carried out for this analysis with dye reversal for every second pair of RNAs.
2010-05-19 | E-GEOD-13056 | biostudies-arrayexpress
Project description:EBNA1 is the EBV-encoded nuclear antigen required for viral episome maintenance during latency. EBNA1 is a sequence specific DNA binding protein with high affinity binding sites for the viral genome, especially OriP. EBNA1 can also bind sequence specifically to a large number of sites in the host cellular genome, but the function of these binding sites has remained elusive. EBNA1 is also known to provide a host cell survival function, but the molecular mechanisms accounting for this function are not completely understood. Here, we show by integrating ChIP-Seq and RNA-Seq with experimental validation that MEF2B, IL6R, and EBF1 are high confidence target genes of EBNA1 that are essential for viability of B-lymphocytes latently infected with EBV. We show that EBNA1 binds to ~1000 sites with many, but not all, universally bound in different cell types, including Burkitt lymphoma (BL) and nasopharyngeal carcinoma (NPC). We find that a large subset of EBNA1 binding sites are located proximal to transcription start sites and correlate genome-wide with transcription activity. EBNA1 bound to genes of high significance for B-cell growth and function, including MEF2B, IL6R, EBF1, RNF145, POU2F1, KDM4C, FGR, EGFR, LAIR, CDC7, CD44, and IL17A. EBNA1 depletion from latently infected LCLs results in the loss of cell proliferation, and the loss of gene expression for some EBNA1-bound genes, including MEF2B, EBF1, and IL6R. Depletion of MEF2B, EBF1, or IL6R partially phenocopies EBNA1-depletion by decreasing EBV-positive cell growth and viability. These findings indicate that EBNA1 binds to a large cohort of cellular genes important for cell viability, and implicates EBNA1 as a master coordinator of host cell gene expression important for enhanced survival of latently infected cells. Examination of EBNA1 binding in Raji, MutuI, LCL and C666-1 cells and EBNA1 knockdown effect on mRNA gene expression in LCL
2015-12-16 | E-GEOD-73887 | biostudies-arrayexpress