Epstein-Barr virus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA794826 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17584881_1.fastq.gz | Fastqsanger.gz | |||
| SRR17584881_2.fastq.gz | Fastqsanger.gz | |||
| SRR17584882_1.fastq.gz | Fastqsanger.gz | |||
| SRR17584882_2.fastq.gz | Fastqsanger.gz | |||
| SRR17584883_1.fastq.gz | Fastqsanger.gz |
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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
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
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
Project description: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.
2023-05-15 | MSV000091949 | MassIVE
Project description:Our appreciation for the extent of Epstein Barr virus (EBV) transcriptome complexity continues to grow through findings of EBV encoded microRNAs, new long non-coding RNAs, and hundreds of new polyadenylated lytic transcripts. Here we report an additional layer to the EBV transcriptome through the identification of a repertoire of latent and lytic viral circRNAs. Utilizing RNase R-sequencing with cell models representing latency types I, II, and III, we identified circRNAs expressed from the latency Cp promoter involving backsplicing from the W1 and W2 exons to the C1 exon, from the EBNA BamHI U exon, and from the latency long-non-coding RPMS1 locus. We also identified circRNAs expressed during reactivation including an exon 8-to-2 backspliced LMP2 transcript and a highly expressed circRNA derived from the BHLF1 gene. Altogether we identified over 30 EBV circRNA candidates and validated and determined the structural features, expression profiles and nuclear-cytoplasmic distributions of several prominent viral circRNAs. Further, we show that two RPMS1 circRNAs are expressed in stomach cancer specimens. This study increases the known EBV latency and lytic transcriptome repertoires to include viral circRNAs and provides an essential foundation for investigations into the functions of this new class of EBV transcripts in EBV biology and disease.
2018-07-12 | GSE116675 | GEO
Project description:Epstein-Barr virus (EBV) is present in a state of latency in infected memory B-cells and EBV-associated lymphoid and epithelial cancers. Cell stimulation or differentiation of infected B-cells and epithelial cells induces reactivation to the lytic replication cycle. In each cell type, the EBV transcription and replication factor Zta (BZLF1, EB1) plays a role in mediating the lytic cycle of EBV. Zta is a transcription factor that interacts directly with Zta response elements (ZREs) within viral and cellular genomes. Here we undertake chromatin-precipitation coupled to DNA-sequencing (ChIP-Seq) of Zta-associated DNA from cancer-derived epithelial cells. The analysis identified over 14,000 Zta-binding sites in the cellular genome. We assessed the impact of lytic cycle reactivation on changes in gene expression for a panel of Zta-associated cellular genes. Finally, we compared the Zta-binding sites identified in this study with those previously identified in B-cells and reveal substantial conservation in genes associated with Zta-binding sites.
2021-02-20 | GSE83354 | GEO
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
Project description: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. ZEBRA then transcriptionally activates other EBV genes and together with some of those gene products ensures completion of the lytic cycle. However, not every latently-infected cell exposed to a lytic trigger turns expression of ZEBRA on, resulting in responsive and refractory subpopulations. What governs this dichotomy? By examining the nascent transcriptome following exposure to a lytic trigger, we find that several cellular genes are transcriptionally upregulated temporally upstream of ZEBRA. These genes regulate lytic susceptibility to variable degrees in latently-infected cells that respond to mechanistically distinct lytic triggers. While increased expression of these cellular genes defines a pro-lytic state, such upregulation also runs counter to the well-known mechanism of viral nuclease-mediated host shut-off that is activated downstream of ZEBRA. Furthermore, a subset of upregulated cellular genes is transcriptionally repressed downstream of ZEBRA, indicating an additional mode of virus-mediated host shut-off through transcriptional repression. Thus, increased transcription of a set of host genes contributes to a pro-lytic state that allows a subpopulation of cells to support the EBV lytic cycle.
2020-01-13 | GSE141220 | GEO
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
Project description:Epstein-Barr Virus (EBV) encoded Nuclear Antigens (EBNAs) and virus activated NF-kB subunits mostly bind to enhancers in EBV transformed lymphoblastoid cells lines (LCLs). Using LCL 3D genome organization map that links EBV enhancers to promoters, we built the most comprehensive virus regulome. EBV regulome contained 1992 genes and enhancers directly linked to them. ~30% of genes essential for LCL growth were linked to EBV enhancers. CRISPR knock out of EBNA2 sites significantly reduced their target gene expression. Additional EBV super-enhancer (ESE) targets including MCL1, IRF4, and EBF were identified. MYC ESEs looping to MYC TSS was dependent on EBNAs. CRISPR deletions of MYC ESEs greatly reduced MYC expression and LCL growth. EBNA3A/3C altered CDKN2A/B spatial organization to suppress senescence. EZH2 inhibition decreased the looping at the CDKN2A/B loci and reduced LCL growth. This study defines the most comprehensive host-pathogen interactions on the spatial organization of chromatin during infection and cancer.
2017-09-01 | GSE101426 | GEO