Peripheral blood gene expression in human experiencing primary EBV infection (Ref8)
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ABSTRACT: 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
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
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.
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.
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.
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.
Project description:Capture-based whole-genome sequencing of Epstein-Barr virus (EBV) was performed in hematological malignancies such as EBV-positive diffuse large B-cell lymphoma, extranodal NK/T-cell lymphoma, and chronic active EBV infection.
Project description:Extensive DNA methylation in promoter regions is observed in gastric cancer with Epstein-barr virus (EBV) infection and EBV infection is the cause to induce this extensive hypermethylaiton phenotype in gastric epithelial cells. From transcriptome analysis, we found that TET2, one of the demethylase enzymes, was downregulated by EBV infection in gastric epithelial cell line MKN7. TET2 was overexpressed in a gastric epithelial cell line, GES1, to see its function and the hydroxymethylation, a byproduct of DNA demethylation, acquired genes by TET2 overexpression and methylation acquired genes by EBV infection were significantly overlapped. These suggested that hydroxymethylation by TET2 could function to keep unmethylated status of genes before EBV infection, and TET2 depression could contribute to methylation acquisition of these target genes after EBV infection.
Project description:Proteomic analysis of cytokines in unstimulated oropharyngeal secretions. Epstein-barr virus (EBV) is a type 1 carcinogen which causes many cancers in humans. Here we explored the cytokine involvement of the EBV replication process in the oropharynx. Cytokine interactomic profiles were geneerated to understand the involved signalling pathways in HIV infected group and the healthy group. Proteome profilers were used to understand the major cytokine expression levels that are related to infection and immune regulation.
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.
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.