A model for persistent infection with Epstein-Barr virus: the stealth virus of human B cells.
about
Epstein-Barr virus provides a new paradigm: a requirement for the immediate inhibition of apoptosis.A gammaherpesvirus Bcl-2 ortholog blocks B cell receptor-mediated apoptosis and promotes the survival of developing B cells in vivoEpstein-Barr virus encoded latent membrane protein 1 (LMP1) and TNF receptor associated factors (TRAF): colocalisation of LMP1 and TRAF1 in primary EBV infection and in EBV associated Hodgkin lymphoma.Identification of closely spaced but distinct transcription initiation sites for the murine gammaherpesvirus 68 latency-associated M2 gene.Biology and disease associations of Epstein-Barr virus.The murine gammaherpesvirus 68 M2 gene is required for efficient reactivation from latently infected B cells.Establishment and maintenance of long-term murine gammaherpesvirus 68 latency in B cells in the absence of CD40.CD4+ T-cell effectors inhibit Epstein-Barr virus-induced B-cell proliferation.Detection of Epstein-Barr virus genomes in peripheral blood B cells from solid-organ transplant recipients by fluorescence in situ hybridization.Pediatric solid-organ transplant recipients carry chronic loads of Epstein-Barr virus exclusively in the immunoglobulin D-negative B-cell compartment.MYC overexpression imposes a nonimmunogenic phenotype on Epstein-Barr virus-infected B cells.Cross-linking of CD80 and CD86 Diminishes Expression of CD54 on EBV-transformed B Cells through Inactivation of RhoA and RasEBV Chronic InfectionsThe immunology of Epstein-Barr virus infectionEpstein-Barr-virus-encoded LMP2A induces primary epithelial cell migration and invasion: possible role in nasopharyngeal carcinoma metastasis.Diagnostic testing in Epstein-Barr virus infection.Human cytomegalovirus gene expression during infection of primary hematopoietic progenitor cells: a model for latency.Latent membrane protein 1 inhibits Epstein-Barr virus lytic cycle induction and progress via different mechanisms.Terminal differentiation into plasma cells initiates the replicative cycle of Epstein-Barr virus in vivo.Modulation of Epstein-Barr virus glycoprotein B (gB) fusion activity by the gB cytoplasmic tail domainThe effects of the Epstein-Barr virus latent membrane protein 2A on B cell function.Immunogenicity of cytopathic and noncytopathic viral vectorsEarly establishment of gamma-herpesvirus latency: implications for immune control.Mapping regions of Epstein-Barr virus (EBV) glycoprotein B (gB) important for fusion function with gH/gL.The Epstein-Barr virus encoded BART miRNAs potentiate tumor growth in vivo.Demonstration of the Burkitt's lymphoma Epstein-Barr virus phenotype in dividing latently infected memory cells in vivo.Long-term latent murine Gammaherpesvirus 68 infection is preferentially found within the surface immunoglobulin D-negative subset of splenic B cells in vivo.Tonsillar memory B cells, latently infected with Epstein-Barr virus, express the restricted pattern of latent genes previously found only in Epstein-Barr virus-associated tumors.The KGD motif of Epstein-Barr virus gH/gL is bifunctional, orchestrating infection of B cells and epithelial cells.Kaposi's sarcoma-associated herpesvirus-infected primary effusion lymphoma has a plasma cell gene expression profile.Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cellsSystematic mutagenesis of the murine gammaherpesvirus 68 M2 protein identifies domains important for chronic infection.Robust in vivo transduction of a genetically stable Epstein-Barr virus episome to hepatocytes in mice by a hybrid viral vectorc-Myc and Rel/NF-kappaB are the two master transcriptional systems activated in the latency III program of Epstein-Barr virus-immortalized B cells.MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs.Functional analysis of glycoprotein L (gL) from rhesus lymphocryptovirus in Epstein-Barr virus-mediated cell fusion indicates a direct role of gL in gB-induced membrane fusion.Surface immunoglobulin-deficient Epstein-Barr virus-infected B cells in the peripheral blood of pediatric solid-organ transplant recipients.EBV Persistence--Introducing the Virus.Thymoquinone efficiently inhibits the survival of EBV-infected B cells and alters EBV gene expression.Cells expressing the Epstein-Barr virus growth program are present in and restricted to the naive B-cell subset of healthy tonsils
P2860
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P2860
A model for persistent infection with Epstein-Barr virus: the stealth virus of human B cells.
description
1999 nî lūn-bûn
@nan
1999 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հունվարին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
A model for persistent infecti ...... tealth virus of human B cells.
@ast
A model for persistent infecti ...... tealth virus of human B cells.
@en
type
label
A model for persistent infecti ...... tealth virus of human B cells.
@ast
A model for persistent infecti ...... tealth virus of human B cells.
@en
prefLabel
A model for persistent infecti ...... tealth virus of human B cells.
@ast
A model for persistent infecti ...... tealth virus of human B cells.
@en
P1433
P1476
A model for persistent infecti ...... tealth virus of human B cells.
@en
P2093
Babcock GJ
Thorley-Lawson DA
P304
P356
10.1016/S0024-3205(99)00214-3
P407
P577
1999-01-01T00:00:00Z