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Gene expression data from human platelets infected by EBV in vitro

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181074 | GEO | 2022/01/01

REPOSITORIES: GEO

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microRNA expression data from human platelets infected by EBV in vitro

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

The viral and cellular microRNA targetome in lymphoblastoid cell lines

Project description:Epstein-Barr virus (EBV) is a human herpesvirus linked to a number of B cell cancers and lymphoproliferative disorders. During latent infection, EBV expresses 25 viral pre-microRNAs (miRNAs) and induces the expression of specific host miRNAs, such as miR-155 and miR-21, which potentially play a role in viral oncogenesis. To date, a limited number of EBV miRNA targets have been identified; thus, the role of EBV miRNAs in viral pathogenesis is not well defined. Here, we used photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) combined with deep sequencing and computational analysis to comprehensively examine the viral and cellular miRNA targetome in EBV B95-8-infected lymphoblastoid cell lines (LCLs). We identified 7,827 miRNA-interaction sites in 3,492 cellular 3'UTRs. 531 of these sites contained seed-matches to viral miRNAs. 24 PAR-CLIP-identified miRNA:3'UTR interactions were confirmed by reporter assays. Our results reveal that EBV miRNAs predominantly target cellular transcripts during latent infection, thereby manipulating the host environment. Furthermore, targets of EBV miRNAs are involved in multiple cellular processes that are directly relevant to viral infection, including innate immunity, cell survival, and cell proliferation. Finally, we present evidence that myc-regulated host miRNAs from the miR-17/92 cluster can regulate latent viral gene expression. This comprehensive survey of the miRNA targetome in EBV-infected B cells represents a key step towards defining the functions of EBV-encoded miRNAs, and potentially, identifying novel therapeutic targets for EBVassociated malignancies. Ago2 (Argonaute 2) PAR-CLIP and small RNA deep sequencing of Epstein-Barr virus B95.8-infected lymphoblastoid cell lines (LCLs).

2012-10-16 | E-GEOD-41437 | biostudies-arrayexpress

Proteomics of EBV-infected lytic and refractory cells

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

Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

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.

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Expression data from Burkitt Lymphoma cell lines followed by expression or inhibition of ebv-BART6-3p microRNA

Project description:Epstein-Barr virus is associated with several human malignancies, including Burkitt Lymnphoma. The virus encodes more than 40 microRNAs, which participate in its possible pathogenetic role. We used microarrays to study the effect of the expression of an Epstein-Barr virus-encoded microRNA (ebv-BART6-3p) on the global gene expression profile of Burkitt Lymphoma cell lines.

2016-03-02 | GSE63665 | GEO

Gene expression profiling of age-related EBV-positive B-cell lymphoproliferative disorders uncovers alterations in characteristic oncogenetic pathways: possible implications for pathogenesis

Project description:Comprehensive gene expression profiles of Epstein-Barr virus (EBV)-associated B cell neoplasm (clinical samples + cell lines)

2014-04-11 | E-MTAB-973 | biostudies-arrayexpress

Establishing a common marmoset induced pluripotent stem cell line NM-iPS by an all-in-one episomal vector approach

Project description:Epstein-Barr virus (EBV)-based episomal vector system enables persistent transgene expression, which is advantageous for efficient derivation of transgene-free induced pluripotent stem cells (iPSCs) without viral transduction. Here, we report establishment of an iPSC line from somatic fibroblasts of a neonatal common marmoset monkey (marmoset; Callithrix jacchus) using an all-in-one episomal vector that we newly developed. The established iPSC line, named NM-iPS, showed standard characteristics of pluripotency such as pluripotency-related marker expression, three germ layer differentiation, and normal karyotype (2n = 46). The novel iPSC line would be a useful resource for stem cell research using non-human primates.

2021-01-10 | GSE164497 | GEO

Peripheral blood gene expression in human experiencing primary EBV infection (Ref8)

Project description:Epstein Barr virus causes linfectious mononucleosis and establishes lifelong infection associated with cancer and autoimmune disease. To better understand immunity to EBV, we performed a prospective study of natural infection in healthy humans. These anlyses were undertaken in order to determine what gene expression changes occur as the result of primary Epstein Barr virus infection. Samples were taken both before and following acquisition of the virus for direct comparison of samples for single subjects. These data provide an important first description of the response to natural herepesvirus infection in humans. PBMC were taken before acquisition of EBV, during acute infection, and during latency

2013-12-31 | E-GEOD-45918 | biostudies-arrayexpress

Peripheral blood gene expression in human experiencing primary EBV infection (HT12)

2013-12-31 | E-GEOD-45919 | biostudies-arrayexpress

circRNA microarray of the Epstein-Barr virus positive Burkitt's lymphoma cell line Akata

Project description:Epstein-Barr virus positive Burkitt's lymphoma cell line Akata (+) and it's EBV-depleted subclone Akata (-) were analyzed for human circRNA expression.

2022-12-19 | GSE206824 | GEO

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