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Project description:AmpliSeq Transcriptome profiling of human B cells from EBV-infected and FK506-treated humanized mice.
| PRJNA522254 | ENA
Project description:To understand epigenic dysregulation of host and viral genes upon EBV infection in human gastric cancer, genome wide transcripts by RNAseq were undertaken for total RNAs of 3 EBVnGC, their isogenic cell lines converted by in vitro EBV-infection and 3 EBV-naturally infected GC cell lines.
2014-09-01 | GSE60873 | GEO
Project description:Purpose: Evaluation of the m6A modification of EBV and BJAB transcripts during EBV infection Methods: Human B lymphoma cell line BJAB was uninfected or infected with EBV for 24 hours. Total RNA from each sample were extracted. Intact mRNA was isolated from total RNA samples and then chemically fragmented to 100-nucleoside-long fragments. m6A methylated mRNAs were immunoprecipitated with anti-N6-methyadenosine (m6A) antibody (a part of the fragmented mRNAs was kept as input). Both m6A enriched mRNAs and input mRNAs were concentrated for RNA-seq library construction. Sequencing was performed using an Illumina HiSeq 4000. Results: EBV EBNA2 and BHRF1 transcripts were m6A modified and m6A modification of BJAB transcripts changed during EBV infection. Conclusions: Our study found that some EBV transcripts were m6A modified during EBV infection and EBV infection changed m6A modification profiles of BJAB transcripts.
2021-07-10 | GSE133936 | GEO
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:In order to gain insights into the intricate molecular alterations taking place following Epstein-Barr virus (EBV) infection in primary B-cells, we employed RNA-Seq to investigate the dynamic changes occurring within the cell transcriptome during the early stages of EBV infection (0, 2, and 4 days post infection). By analysing the transcriptomic data generated, our objective was to find novel pathways and mechanisms that may play pivotal roles in the EBV-induced transformation of B-cells, particularly during early stage of B-cell activation.
2023-08-03 | GSE235941 | GEO
Project description:There is evidence for the beneficial effect of FK506, an effective immunosuppressive agent, for the treatment of asthma; however, the mechanisms underlying these effects are unclear. Using a mouse model of airway inflammation induced by Papain, a protease allergen, and RNAseq analysis of lung innate cells, we found that FK506 inhibited the activation of ILC2s, which initiate airway inflammation, as well as the induction of TH2 cells, which cause chronic inflammation. Our findings further support the clinical value of FK506 for the treatment of allergen-induced airway inflammation and clarify its targets and mechanisms of action.
2021-12-07 | GSE189918 | GEO
Project description:Cells were grown in YPD medium (pH 5.0) at 30oC to a density of 0.6 X 107 cells/ml (A600=0.6). The culture was supplemented with FK506 (1.0 mg/ml) in ET at 30oC for 15 min. Cells were collected for the t=0 min sample. Next, an equal volume of YPD medium (pH 5.0) containing FK506 (1.0 mg/ml) and 1.6 M NaCl was added to the FK506-treated culture (final concentration 0.8 M NaCl). Samples were collected 15, 30, 45 and 60 minutes after Na+ addition.
2005-01-01 | E-SMDB-14 | biostudies-arrayexpress
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:Post-transplant lymphoproliferative disorder (PTLD) is a potentially fatal complication after organ transplantation frequently associated with the Epstein-Barr virus (EBV). Immunosuppressive treatment is thought to allow the expansion of EBV-infected B cells, which often express all eight oncogenic EBV latent proteins. Here, we assessed whether HLA-A2 transgenic humanized NSG mice treated with the immunosuppressant FK506 could be used to model EBV-PTLD. We found that FK506 treatment of EBV-infected mice led to an elevated viral burden, more frequent tumor formation and diminished EBV-induced T cell responses, indicative of reduced EBV-specific immune control. EBV latency III and lymphoproliferation-associated cellular transcripts were up-regulated in B cells from immunosuppressed animals, akin to the viral and host gene expression pattern found in EBV-PTLD. Utilizing an unbiased gene expression profiling approach, we identified genes differentially expressed in B cells of EBV-infected animals with and without FK506 treatment. Upon investigating the most promising candidates, we validated sCD30 as a marker of uncontrolled EBV proliferation in both humanized mice and in pediatric patients with EBV-PTLD. High levels of sCD30 have been previously associated with EBV-PTLD in patients. As such, we believe that humanized mice can indeed model aspects of EBV-PTLD development and may prove useful for the safety assessment of immunomodulatory therapies.
| S-EPMC7162544 | biostudies-literature
Project description:Extranodal NK/T-cell, nasal type (hereinafter, nasal T/NK lymphoma), is a distinct clinicopahtologic entity highly associated with EBV. Among nasal T/NK lymphoma, some cases are developed from the long-lasting EBV infection termed chronic active EBV (CAEBV) infection.The clonal expansion of EB infected T- or NK cell are seen in patients with both nasal T/NK lymphoma and CAEBV infection, suggesting that two diseases might partly share the similar mechanism by which EBV affect host cellular genes. Question has thus arisen why a subset of patients with CAEB infection develop into nasal T/NK lymphoma. This study aimed to investigate the virus-host interaction in EBV-associated lymphoma. Keywords = nasak NK/T lymphoma Keywords = chronic active EBV infection Keywords: other
2006-01-11 | GSE2432 | GEO