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JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta Brd4 ChIP-seq]

ABSTRACT: Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The ChIP-seq data below show that the BET proteins bind to both EBV lytic origins of replication.

ORGANISM(S): Homo sapiens human gammaherpesvirus 4

PROVIDER: GSE98773 | GEO | 2017/06/30

SECONDARY ACCESSION(S): PRJNA386167

REPOSITORIES: GEO

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JQ1 prevents BRD4 recruitment to the lytic origins of replication [Akata-Zta DNA-seq]

2017-06-30 | GSE98772 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data below show that JQ1 and I-BET cause a decrease in EBV genome replication after induction.

2017-06-30 | GSE84212 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the second block causes a decrease in expression of late but not early lytic genes.

2017-06-30 | GSE84211 | GEO

BET proteins bind the lytic origins of replication [MutuI ChIP-seq]

2017-06-30 | GSE84213 | GEO

BET inhibitors suppress BZLF1 expression [MutuI DNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The sequenced total DNA data in this series show that JQ1 causes a decrease in EBV genome replication upon antibody induction.

2017-06-30 | GSE84210 | GEO

Ceramide Promotes Lytic Reactivation of Epstein-Barr Virus in Gastric Carcinoma

Project description:Epstein-Barr virus (EBV) has a lifelong latency period after initial infection. Rarely, however, when the EBV immediate early gene BZLF1 is expressed by a specific stimulus, the virus switches to the lytic cycle to produce progeny viruses. We found that EBV infection reduced levels of various ceramide species in gastric cancer cells. As ceramide is a bioactive lipid implicated in the infection of various viruses, we assessed the effect of ceramide on the EBV lytic cycle. Treatment with C6-ceramide (C6-Cer) induced an increase in the endogenous ceramide pool and increased production of the viral product as well as BZLF1 expression. Treatment with the ceramidase inhibitor ceranib-2 induced EBV lytic replication with an increase in the endogenous ceramide pool. The glucosylceramide synthase inhibitor Genz-123346 inhibited C6-Cer-induced lytic replication. C6-Cer induced ERK1/2 and CREB phosphorylation, c-JUN expression, and accumulation of the autophagosome marker LC3B. Treatment with MEK1/2 inhibitor U0126 or autophagy initiation inhibitor 3-MA suppressed C6-Cer-induced EBV lytic replication. In contrast, the autophagosome-lysosome fusion inhibitor chloroquine induced BZLF1 expression. Transfection with siCREB reduced ERK1/2 phosphorylation and C6-Cer-induced BZLF1 expression. On the other hand, siJUN transfection did not affect BZLF1 expression. Our results show that increased endogenous ceramide and glycosyl ceramide (GlyCer) following C6-Cer treatment induce EBV lytic replication in gastric cancer cells via ERK1/2 and CREB phosphorylation and autophagosome accumulation.

2023-12-20 | MTBLS7649 | MetaboLights

BET inhibitors suppress BZLF1 expression [MutuI RNA-seq]

Project description:Lytic infection by the Epstein-Barr virus (EBV) poses numerous health risks, such as infectious mononucleosis and lymphoproliferative disorder. We demonstrate that JQ1 and other BET inhibitors block two different steps in the sequential cascade of the EBV life cycle: expression of the immediate-early gene BZLF1 and lytic genome replication. This represents a novel mode of action for antiviral drugs that may increase efficacy and decrease emergence of resistance. The RNA-seq data below show that the first block by JQ1 occurs before transcription of any EBV lytic genes (see wigs of EBV transcriptomes). A subset of the same RNA-seq data (three replicates each of Mutu+vehicle was compared to Mutu+JQ1) was examined for changes in the human transcriptome, and those results are presented in the spreadsheet "Differential_Expression_GEO"

2017-06-30 | GSE84209 | GEO

BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta DNA-seq]

| PRJNA328410 | ENA

BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

Project description:BET inhibitors suppress lytic DNA replication [Akata-Zta RNA-seq]

| PRJNA328406 | ENA

¬¬Identifying the cellular interactome of Epstein-Barr virus lytic regulator Zta reveals cellular targets contributing to viral replication.

Project description:The human gamma herpesvirus Epstein-Barr virus, infects most adults and is an important contributor to the development of many types of cancer. Essential contributions of viral genes to replication are known but the potential contributions of cell genes to viral replication are less well delineated. A key player is the viral protein Zta (BZLF1, ZEBRA, Z). This sequence-specific DNA-binding protein can disrupt viral latency by driving the transcription of target genes and by interacting with the EBV lytic origin of replication. Here we used an unbiased approach to identify the Zta-interactome in cells derived from a Burkitt’s lymphoma. Isolating Zta and associated proteins from Burkitt’s lymphoma cells undergoing EBV replication, followed by Tandem Mass Tag (TMT) mass spectrometry resulted in the identification of forty-four viral and cellular proteins in the Zta interactome. Of these two were known targets of Zta. The association of Zta with Hsc70 and the contribution that Hsc70 plays to EBV replication mirrors a contribution from HSP70 family members to the replication of other herpesviruses. Conversely, the association of Zta with NFATc2 has no known parallels for other herpesviruses. Zta attenuates the activity of an NFAT-dependent promoter, which shows a potential for dampening the expression of genes regulated by calcium-dependent signal transduction. Indeed, Zta has the ability to affect a feed-back loop limiting its own expression, which would aid viral replication by preventing the toxic effects of Zta overexpression.

2019-06-06 | PXD013727 | Pride

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