Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA360825 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:<p>Following infection of B cells, Epstein Barr virus (EBV) engages host pathways that mediate cell proliferation and transformation, contributing to the propensity of the virus to drive immune dysregulation and lymphomagenesis. We found that the EBV protein EBNA2 initiates NAD <em>de novo</em> biosynthesis by driving expression of the host metabolic enzyme IDO1. Virus-enforced NAD production sustained mitochondrial complex I activity, to match ATP-production with bioenergetic requirements of proliferation and transformation. In transplant patients, IDO1 expression in EBV-infected B cells, and a serum signature of increased IDO1 activity, preceded development of lymphoma. In humanized mice infected with EBV, IDO1 inhibition reduced both viremia and lymphomagenesis. Virus-orchestrated NAD biosynthesis is thus a druggable metabolic vulnerability of EBV-driven B cell transformation – opening therapeutic possibilities for EBV-related diseases.</p>
2024-04-29 | MTBLS2243 | MetaboLights
Project description:Most humans are infected with Epstein-Barr virus (EBV), a cancer-causing virus. While EBV generally persists silently in B lymphocytes, periodic lytic (re-)activation of latent virus is central to its life cycle and to most EBV-related diseases. However, a substantial fraction of EBV-infected B cells and tumor cells in a population is refractory to lytic activation. This resistance to lytic activation directly and profoundly impacts viral persistence and effectiveness of oncolytic therapy for EBV+ cancers. To identify the mechanisms that underlie susceptibility to EBV-lytic activation, we used host protein-expression profiling of separated-lytic and -refractory cells.
2016-04-27 | PXD001838 | Pride
Project description:Most humans are infected with Epstein-Barr virus (EBV), a cancer-causing virus. While EBV generally persists silently in B lymphocytes, periodic lytic (re-)activation of latent virus is central to its life cycle and to most EBV-related diseases. However, a substantial fraction of EBV-infected B cells and tumor cells in a population is refractory to lytic activation. This resistance to lytic activation directly and profoundly impacts viral persistence and effectiveness of oncolytic therapy for EBV+ cancers. To identify the mechanisms that underlie susceptibility to EBV-lytic activation, we used host protein-expression profiling of separated-lytic and -refractory cells.
2016-07-22 | MSV000079993 | MassIVE
Project description:Gene expression profile of AGS gastric carcinoma cell line infected in vitro with Epstein-Barr Virus. Some samples also contain are stably transfected with a dominant negative LMP1 construct. 8 total samples. 4 biological replicates of EBV infected cells, 2 biological replicates with EBV infected cells with LMP1DN construct, and 2 biological replicates with EBV infected cells with control vector.
2012-05-07 | E-GEOD-37753 | biostudies-arrayexpress
Project description:Viruses can directly interact with platelets and modulate their function. Viral impact on platelet activation, and platelet-mediated modulations of innate and adaptive immune responses. Human herpesvirus 4, also known as Epstein–Barr virus (EBV) interaction with platelets occurs via complement receptor 2 (CR2), but the exact mechanism of action with platelets is still poorly understood. Epstein–Barr virus (EBV), is extremely efficient at establishing a persistent life-long infection in human B cells. In the present study, GeneChips were performed in human platelets from three normal donors infected with the EBV-containing supernatant of the B95.8 marmoset cell line in vitro.
2022-01-01 | GSE181074 | GEO
Project description:Viruses can directly interact with platelets and modulate their function. Viral impact on platelet activation, and platelet-mediated modulations of innate and adaptive immune responses. Human herpesvirus 4, also known as Epstein–Barr virus (EBV) interaction with platelets occurs via complement receptor 2 (CR2), but the exact mechanism of action with platelets is still poorly understood. Epstein–Barr virus (EBV), is extremely efficient at establishing a persistent life-long infection in human B cells. In the present study, GeneChips were performed in human platelets from three normal donors infected with the EBV-containing supernatant of the B95.8 marmoset cell line in vitro.
2022-01-01 | GSE181075 | GEO
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
Project description:Small RNA-Seq study comparing Epstein-Barr virus (EBV) infected BJAB-B1 cells to isogenic, but uninfected, BJAB cells. The goal was to deduce differentially expressed small ncRNAs both micro and non-micro (up to 200 nt) between the two cell lines to gain insights into EBV-associated deregulation of host small ncRNAs.
2019-10-26 | GSE139425 | GEO
Project description:Genome wide association studies have identified >200 susceptibility loci accounting for much of the heritability of Multiple Sclerosis (MS). Epstein-Barr virus (EBV), a memory B cell tropic virus, has been identified as necessary but not sufficient for development of MS. The molecular and immunological basis for this has not been established. Infected B cell proliferation is driven by signalling through the EBV produced cell surface protein LMP1, a homologue of the MS risk gene CD40. Methods: We have investigated transcriptomes of B cells and EBV infected B cells at Latency III (LCLs) and identified MS risk genes with altered expression on infection
2019-04-01 | GSE126379 | 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