GEO DataSets

(Submitter supplied) 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.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

23 Samples

Download data: BW

(Submitter supplied) We used Precision Nuclear Run-on followed by Deep Sequencing (PRO-Seq) to investigate RNA Polymerase (Pol) activity during Epstein-Barr Virus (EBV) reactivation and its link to CTCF in latently EBV infected ymphoblastoid cell lines (LCLs). Nuclei were harvested from WT LCLs or LCLs containing an 18bp deletion at the LMP CTCF binding site (DCTCF) treated with DMSO or induced to reactivate with the small molecule C60 for 24h. more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL21697

8 Samples

Download data: BW

(Submitter supplied) Epstein Barr Virus (EBV) is a potentially oncogenic gammaherpesvirus that establishes a chronic, latent infection in memory B cells. The EBV genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type. CTCF is post-translationally modified by the host enzyme PARP1. more...

Organism:

human gammaherpesvirus 4

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL25190

8 Samples

Download data: BED, BEDGRAPH, BW, NARROWPEAK

(Submitter supplied) RNAseq was used to identify host and EBV viral transcriptome changes in CHAF1B knock-out Akata EBV+ cells. CHAF1B KO Akata EBV+ cells were subjected to RNAseq analysis. The Akata EBV+ cells expressing control sgRNA was used as the control.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

6 Samples

Download data: CSV

(Submitter supplied) Using strand specific RNA-seq to assess the EBV transcriptome during reactivation of Akata cells, we found extensive bidirectional transcription extending across nearly the entire genome.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

13 Samples

Download data: WIG

(Submitter supplied) Lytic activation from latency is a key transition point in the life cycle of herpesviruses. Epstein-Barr virus (EBV) is a human herpesvirus that can cause lymphomas, epithelial cancers, and other diseases, most of which require the lytic cycle. While the lytic cycle of EBV can be triggered by chemicals and immunologic ligands, the lytic cascade is only activated when expression of the EBV latency-to-lytic switch protein ZEBRA is turned on. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Other

Platform:

GPL16791

12 Samples

Download data: TXT

(Submitter supplied) RNA profile changes in primary resting B cells after EBV infection

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

21 Samples

Download data: CSV

(Submitter supplied) 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.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

12 Samples

Download data: TXT

(Submitter supplied) As a human tumor virus, EBV is present as a latent infection in its associated malignancies where genetic and epigenetic changes have been shown to impede cellular differentiation and viral reactivation. One such change is increased levels of the Wnt signaling effector, lymphoid enhancer binding factor 1 (LEF1) following EBV epithelial infection. In silico analysis of EBV type 1 and 2 genomes identified over 20 Wnt-response elements suggesting that LEF1 may directly bind the EBV genome and regulate the viral life cycle. more...

Organism:

human gammaherpesvirus 4

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL33849 GPL33850

31 Samples

Download data: BEDGRAPH

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

30 Samples

Download data

(Submitter supplied) RNAseq was used to identify host and viral transcriptome changes in xenograft tumors treated with DMSO or CBL0137. Mouse xenograft experiments were regulated by Institutional Animal Care & Use Committee (IACUC# 2017-0035) of Weill Cornell Medical Center(WCMC). Non-obese diabetic/severe combined immunodeficiency (NOD-SCID) mice were obtained from Jackson Laboratories. Six to eight-week-old male and female mice (10 male/18 female) were injected in the flank with 1 x 107 BL cells in PBS with Matrigel eleven days before the treatment. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

6 Samples

Download data: XLSX

(Submitter supplied) To gain insights into how EBV latency is maintained, we performed a human genome-wide CRISPR screen in latently EBV-infected Burkitt lymphoma B-cells. Our analyses identified a network of host factors that repress EBV lytic reactivation, centered on the transcription factor MYC and including cohesins, FACT, STAGA and Mediator. RNAseq was used to identify host and viral transcriptome changes in P3HR-1 Burkitt lymphoma cells expressing control, smc1a, supt16h, med12, or tada2b sgRNAs. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

24 Samples

Download data: CSV

(Submitter supplied) Chromatin-organizing factors, like CTCF and cohesins, have been implicated in the control of complex viral regulatory programs. We investigated the role of CTCF and cohesin in the control of the latent to lytic switch for Kaposi's Sarcoma-Associated Herpesvirus (KSHV). We found that cohesin subunits, but not CTCF, were required for the repression of KSHV immediate early gene transcription. Depletion of cohesin subunits Rad21, SMC1, or SMC3 resulted in lytic cycle gene transcription and viral DNA replication. more...

Organism:

Homo sapiens; Human gammaherpesvirus 8

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL9115 GPL15642

5 Samples

Download data: BED, WIG

(Submitter supplied) CTCF and the cohesin complex modify chromatin by binding to DNA and interacting with each other and with other cellular proteins. Both proteins regulate transcription by a variety of local effects on transcription and by long range topological effects. CTCF and cohesin also bind to herpesvirus genomes at specific sites and regulate viral transcription during latent and lytic cycles of replication. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

9 Samples

Download data: TXT

(Submitter supplied) CTCF and the cohesin complex modify chromatin by binding to DNA and interacting with each other and with other cellular proteins. Both proteins regulate transcription by a variety of local effects on transcription and by long range topological effects. CTCF and cohesin also bind to herpesvirus genomes at specific sites and regulate viral transcription during latent and lytic cycles of replication. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

9 Samples

Download data: BW

(Submitter supplied) Epstein-Barr virus (EBV) episome is known to interact with the three-dimensional structure of human genome in infected cells. However, the exact locations of these interactions and their potential functional consequences remain unclear. Recently the high-resolution chromatin interaction capture (Hi-C) assays in lymphoblastoid cells have become available enabling us to precisely map the contacts between the EBV episome(s) and the human host genome. more...

Organism:

Homo sapiens

Type:

Other

Platform:

GPL11154

2 Samples

Download data: BED

(Submitter supplied) Epstein-Barr virus (EBV) establishes life-long latency in human B-cells by maintaining its chromatinized episomes within the nucleus. These circularized mini-chromosomes do not integrate into the host genome. Therefore, it is essential for EBV to organize its chromatin in a manner suitable for genomic stability, DNA replication, and efficient gene expression. Poly [ADP-ribose] polymerase 1 (PARP1) activity is significantly higher in B-cells infected with EBV than those without, and considerably higher in the transcriptionally active type III latency compared to the immunoevasive type I. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL16791 GPL18573

8 Samples

Download data: BW, TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

human gammaherpesvirus 4; Homo sapiens

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL9052 GPL25190

16 Samples

Download data: BEDGRAPH, BROADPEAK, BW

(Submitter supplied) PARP does have an essential role in the regulation of global EBV episome chromatin structure. We have functionally characterized the effect of PARP enzymatic inhibition on total episomal structure and we mapped intragenomic contact changes after PARP inhibition to global binding of the chromatin looping factors CTCF and cohesin across the EBV genome. The altered expression profile after the structural rearrangement induced by PARP inhibition supports the model where PARP1 helps maintain EBV latency programs.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9052

8 Samples

Download data: CSV

(Submitter supplied) PARP does have an essential role in the regulation of global EBV episome chromatin structure. We have functionally characterized the effect of PARP enzymatic inhibition on total episomal structure and we mapped intragenomic contact changes after PARP inhibition to global binding of the chromatin looping factors CTCF and cohesin across the EBV genome. The altered expression profile after the structural rearrangement induced by PARP inhibition supports the model where PARP1 helps maintain EBV latency programs.

Organism:

human gammaherpesvirus 4

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL25190

8 Samples

Download data: BEDGRAPH, BROADPEAK, BW