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RNA-seq detects pharmacological inhibition of Epstein-Barr virus late transcription during spontaneous reactivation.

ABSTRACT: RNA-seq detects pharmacological inhibition of Epstein-Barr virus late transcription during spontaneous reactivation.

OTHER RELATED OMICS DATASETS IN: GSE96689

PROVIDER: PRJNA379377 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5349540.fastq.gz	Fastqsanger.gz
	SRR5349541.fastq.gz	Fastqsanger.gz
	SRR5349542.fastq.gz	Fastqsanger.gz
	SRR5349544.fastq.gz	Fastqsanger.gz
	SRR5349545.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-seq detects pharmacological inhibition of Epstein-Barr virus late transcription during spontaneous reactivation.

Project description:The stepwise and sequential expression of viral genes underlies progression of the infectious life cycle. The Epstein-Barr virus (EBV) is both a tractable model for elucidating principles of transcription as well as a global health threat. We describe an experimental protocol and bioinformatics pipeline for functional identification of EBV true late genes, the last step of transcription prior to virion packaging and egress. All data have been uploaded to the Gene Expression Omnibus under accession code GSE96689. The key improvement over previous approaches is leveraging the sensitivity of RNA-seq to detect gene expression changes during spontaneous reactivation.

2017-07-09 | GSE96689 | GEO

Changes in cellular transcriptome in response to inhibitors of Epstein-Barr virus

Project description:Burkitt lymphoma cells can be latently infected with Epstein-Barr virus (EBV). The virus may be activated into its lytic cycle by small molecules, such as sodium butyrate. Other molecules, such as valproate and valpromide, block viral lytic reactivation. These pharmacological agents alter the cellular physiology that controls viral lytic gene expression. Changes in the cellular transcription were measured in response to one activator and two inhibitors of the Epstein-Barr virus lytic cycle in order to identify cellular genes that are potential regulators of the viral life cycle.

2024-03-13 | GSE135794 | GEO

Richter transfromation of chronic lymphocytic leukemia driven by Epstein-Barr virus reactivation during therapy-realted immunosuppression

Project description:Gene expression analysis in Epstein-Barr virus negative DLBCL samples obtained from patients with Richter syndrome, lymphocytes from CLL patients and epstein-Barr virus positive DLBCL cell lines derived after CLL tumors xenotransplantation

2020-08-29 | GSE103265 | GEO

Increased RNA Polymerase Activity at CTCF binding sites on the Epstein Barr Virus Genome During Reactivation from Latency

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

Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

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.

| 2005372 | ecrin-mdr-crc

Temporal Analysis of Cell Protein Ubiquitination during Epstein-Barr Virus Reactivation by BCR Cross-linking

Project description:Epstein-Barr virus (EBV) reactivation in latently infected B cells is essential for persistent infection and B cell receptor (BCR) activation is a physiologically relevant stimulus for EBV reactivation. Post-translational modifications, such as phosphorylation and ubiquitination, are known to be regulated by antigen binding to BCR within minutes. However, a detailed understanding of the signaling alterations at later time when EBV is being actively replicated remains elusive. To gain insights into BCR activation-mediated reprogramming of the cellular environment in both Akata-BX1 (EBV+) and Akata-4E3 (EBV-) B cells, we utilized a 3-plex stable isotope labeling by amino acid in cell culture (SILAC)-based quantitative proteomic approach to monitor the dynamic changes of protein ubiquitination during the course of immunoglobulin G (IgG) cross-linking of BCRs. We observed temporal alterations in the level of ubiquitination on approximately 150 sites in both Akata-BX1 (EBV+) and Akata-4E3 (EBV-) B cells post-IgG cross-linking compared with no cross-linking controls, with the majority of protein ubiquitination down-regulated. Our analysis revealed that IgG cross-linking plays a major role in the regulation of protein ubiquitination in both EBV+ and EBV- B cells. Bioinformatic analyses of up-regulated ubiquitination events revealed significant enrichment of proteins involved in RNA processing. Among the down-regulated ubiquitination events are proteins enriched in apoptosis and the ubiquitin-proteasome pathway. The comparative and quantitative studies provide a foundation for further understanding how BCR activation regulates cellular protein ubiquitination and how EBV utilizes or subverts BCR engagement-mediated changes to facilitate viral replication.

2017-02-02 | PXD004562 | Pride

The Epstein-Barr virus episome maneuvers between nuclear chromatin compartments during reactivation

Project description:The Epstein-Barr virus episome maneuvers between nuclear chromatin compartments during reactivation

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Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression

Project description:Viral infection leads to heterogeneous cellular outcomes ranging from resistance to virion amplification and cell death. In this study, we apply single-cell techniques to analyze diverse fate trajectories during Epstein-Barr virus (EBV) lytic reactivation in three B cell models. We expand upon the previous finding that c-Myc regulates lytic reactivation and determine that MYC downregulation during the lytic phase is correlated with a loss of germinal center (GC) B cell expression signatures. Consistent with prior work, lytic induction yields both abortive and complete reactivation. Abortive lytic cells, which express high STAT3 and initiate but do not complete the lytic cycle, also upregulate NF-kB and IRF3 pathway target genes. Cells that proceeded through the full lytic cycle exhibited unexpected and striking expression of genes associated with cellular reprogramming, developmental progenitor phenotypes, and cytokine upregulation. Distinct subpopulations of lytic cells further displayed variable profiles for transcripts known to escape virus-mediated host shutoff. These data reveal previously unknown and promiscuous outcomes of lytic reactivation with broad implications for viral replication and EBV-associated oncogenesis.

2024-10-31 | GSE272763 | GEO

Single-Cell Transcriptomics of Epstein-Barr Virus and Human Herpesvirus 6 Coinfection

Project description:Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) infection is widespread among people. Here I describe single-cell RNA sequencing of two lymphoblastoid cell lines harboring both episomal EBV and inherited chromosomally integrated HHV-6. Rare instances of HHV-6 expression appear enriched with EBV reactivation.

2023-05-24 | GSE230239 | GEO

The Epstein-Barr virus episome maneuvers between nuclear chromatin compartments during reactivation [DNA-seq]

Project description:Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.

2017-11-13 | GSE98498 | GEO

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