Long-term latent murine Gammaherpesvirus 68 infection is preferentially found within the surface immunoglobulin D-negative subset of splenic B cells in vivo.
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Gamma-herpesvirus latency requires T cell evasion during episome maintenanceEpstein-Barr virus provides a new paradigm: a requirement for the immediate inhibition of apoptosis.Does EBV alter the pathogenesis of malaria?A virtual look at Epstein-Barr virus infection: biological interpretationsInterplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the HostA gammaherpesvirus Bcl-2 ortholog blocks B cell receptor-mediated apoptosis and promotes the survival of developing B cells in vivoCharacterization of omental immune aggregates during establishment of a latent gammaherpesvirus infectionTracking murine gammaherpesvirus 68 infection of germinal center B cells in vivoGammaherpesvirus-driven plasma cell differentiation regulates virus reactivation from latently infected B lymphocytes.Murine gamma-herpesvirus 68 latency protein M2 binds to Vav signaling proteins and inhibits B-cell receptor-induced cell cycle arrest and apoptosis in WEHI-231 B cells.Effective control of chronic gamma-herpesvirus infection by unconventional MHC Class Ia-independent CD8 T cells.Antibody-independent control of gamma-herpesvirus latency via B cell induction of anti-viral T cell responses.Inhibition of NF-kappaB activation in vivo impairs establishment of gammaherpesvirus latency.The Gammaherpesvirus m2 protein manipulates the Fyn/Vav pathway through a multidocking mechanism of assemblyThe MHV68 M2 protein drives IL-10 dependent B cell proliferation and differentiationIdentification of closely spaced but distinct transcription initiation sites for the murine gammaherpesvirus 68 latency-associated M2 gene.A single CD8+ T cell epitope sets the long-term latent load of a murid herpesvirusExperimental infection of laboratory-bred bank voles (Myodes glareolus) with murid herpesvirus 4.Perturbation of lytic and latent gammaherpesvirus infection in the absence of the inhibitory receptor CEACAM1Expansion of murine gammaherpesvirus latently infected B cells requires T follicular help.Mature and functional viral miRNAs transcribed from novel RNA polymerase III promoters.MHV68 complement regulatory protein facilitates MHV68 replication in primary macrophages in a complement independent manner.Virus-encoded microRNAs facilitate gammaherpesvirus latency and pathogenesis in vivoEx vivo stimulation of B cells latently infected with gammaherpesvirus 68 triggers reactivation from latencyPathogenesis of a model gammaherpesvirus in a natural hostThe 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.Role of B-cell proliferation in the establishment of gammaherpesvirus latency.Murine gammaherpesvirus 68 LANA is essential for virus reactivation from splenocytes but not long-term carriage of viral genome.Inhibition of NF-kappaB signaling reduces virus load and gammaherpesvirus-induced pulmonary fibrosisViral latency and its regulation: lessons from the gamma-herpesviruses.Tyrosine 129 of the murine gammaherpesvirus M2 protein is critical for M2 function in vivoMurine gammaherpesvirus 68 infection is associated with lymphoproliferative disease and lymphoma in BALB beta2 microglobulin-deficient miceA gammaherpesvirus 68 gene 50 null mutant establishes long-term latency in the lung but fails to vaccinate against a wild-type virus challenge.Identification of spliced gammaherpesvirus 68 LANA and v-cyclin transcripts and analysis of their expression in vivo during latent infectionMyeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.Activation of Vav by the gammaherpesvirus M2 protein contributes to the establishment of viral latency in B lymphocytesChemokine binding protein M3 of murine gammaherpesvirus 68 modulates the host response to infection in a natural hostEarly establishment of gamma-herpesvirus latency: implications for immune control.Gammaherpesvirus small noncoding RNAs are bifunctional elements that regulate infection and contribute to virulence in vivo
P2860
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P2860
Long-term latent murine Gammaherpesvirus 68 infection is preferentially found within the surface immunoglobulin D-negative subset of splenic B cells in vivo.
description
2003 nî lūn-bûn
@nan
2003 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@ast
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@en
type
label
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@ast
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@en
prefLabel
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@ast
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@en
P2860
P1433
P1476
Long-term latent murine Gammah ...... et of splenic B cells in vivo.
@en
P2093
David O Willer
Samuel H Speck
P2860
P304
P356
10.1128/JVI.77.15.8310-8321.2003
P407
P577
2003-08-01T00:00:00Z