Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Syncytin1 sequesters viral LF2 to enhance the Epstein-Barr virus lytic phase

ABSTRACT: Previously, we identified Syncytin1 to be expressed in human B cells and enhance EBV ability to undergo lytic replication. To gain mechanistic insight, we performed liquid chromatography tandem mass spectrometry (LC-MS/MS) on tryptic peptides from immunoprecipitated FLAG-tagged Syncytin-1 in latently infected EBV+ Burkitt lymphoma cells. This revealed a number of cellular proteins as potential Syncytin-1 interacting partners during latency and/or during the lytic phase as well as two EBV lytic phase proteins, the viral protein kinase and LF2, a negative regulator of EBV lytic gene transcription. We now find that Syncytin1 reduces the association between LF2 and the EBV replication and transcription activator to promote EBV lytic gene expression.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Human Herpesvirus 4 (strain B95-8) (ncbitaxon:10377) Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Michael T. McIntosh, Ph.D.

PROVIDER: MSV000091949 | MassIVE | Mon May 15 12:30:00 BST 2023

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B-cells

Project description:Epstein Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B-cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain novel insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B-cell proteome and EBV virome. Our approach revealed EBV-induced remodelling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B-cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi sarcoma associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.

2017-05-19 | PXD006317 | Pride

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

Signal Transducer and Activator of Transcription 3 limits Epstein-Barr virus lytic-activation in B lymphocytes.

Project description:We used microarrays to identify genes differentially expressed in EBV-infected human B cells supporting lytic replication vs. those refractory to EBV lytic replication. We used serum from EBV-positive subject (compared to serum from EBV-negative subject) to FACS-separate lytic and refractory cells following treatment of HH514-16 cells with NaB, a lytic cycle inducing agent. RNA from sorted-lytic and sorted-refractory cells were hybridized to microarray.

2013-08-21 | E-GEOD-49568 | biostudies-arrayexpress

Understanding differential expression of genes during EBV lytic cycle reactivation by employing high throughput RNA-sequencing

Project description:To understand the changes in global transcriptomic landscape during the EBV lytic cycle reactivation from lymphoblastoid cell lines (LCLs), RNA-seq was performed. By examining the transcriptomic changes, we obtained valuable insights into the molecular events and regulatory mechanisms involved in EBV reactivation into lytic cycle replication. The study also enhances our knowledge of the complex interplay between EBV and the host cells during its lytic cycle.

2023-08-03 | GSE237484 | GEO

Signal Transducer and Activator of Transcription 3 limits Epstein-Barr virus lytic-activation in B lymphocytes.

Project description:We used microarrays to identify genes differentially expressed in EBV-infected human B cells supporting lytic replication vs. those refractory to EBV lytic replication.

2013-08-21 | GSE49568 | GEO

BET proteins bind the lytic origins of replication [MutuI ChIP-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 ChIP-seq data below show that the BET proteins bind to both EBV lytic origins of replication.

2017-06-30 | GSE84213 | GEO

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

Effect of Effect of lytic replication on EBV and cell gene expression

Project description:The effect of Epstein Barr virus replication on cellular gene expression was studied using AGSiZ epithelial cells which are derived from a gastric carcinoma. The cell line is infected with a recombinant strain of EBV known as Akata BX-1. The cell line was further stably transduced with an inducible EBV Zta transactivator gene. When cells are treated with doxycycline, robust lytic replication of EBV is achieved. Cells made permissive for lytic replication in this manner were harvested for RNA suitable for deep sequencing at 24 and 48 hours post induction in parallel with cells that were mock induced with doxycycline to serve as a control for cells not undergoing EBV replication.

2021-04-15 | GSE155811 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data