Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cells - Wikidata - awgldk - TriplyDB

Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cells

Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cells

http://www.wikidata.org/entity/Q36371017

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Promotion of tumorigenesis by heterozygous disruption of the beclin 1 autophagy gene Gamma-herpesvirus latency requires T cell evasion during episome maintenance Epstein-Barr virus provides a new paradigm: a requirement for the immediate inhibition of apoptosis.Defining immune engagement thresholds for in vivo control of virus-driven lymphoproliferation Murid herpesvirus-4 exploits dendritic cells to infect B cells Crystal Structure of the Gamma-2 Herpesvirus LANA DNA Binding Domain Identifies Charged Surface Residues Which Impact Viral Latency Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host Murine gammaherpesvirus 68 encoding open reading frame 11 targets TANK binding kinase 1 to negatively regulate the host type I interferon response A gammaherpesvirus Bcl-2 ortholog blocks B cell receptor-mediated apoptosis and promotes the survival of developing B cells in vivo Bats, Primates, and the Evolutionary Origins and Diversification of Mammalian Gammaherpesviruses 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 assembly A single CD8+ T cell epitope sets the long-term latent load of a murid herpesvirus Gammaherpesvirus latency induces antibody-associated thrombocytopenia in mice.Experimental 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 CEACAM1 A novel Cre recombinase imaging system for tracking lymphotropic virus infection in vivo.Mature and functional viral miRNAs transcribed from novel RNA polymerase III promoters.Virus-encoded microRNAs facilitate gammaherpesvirus latency and pathogenesis in vivo Ex vivo stimulation of B cells latently infected with gammaherpesvirus 68 triggers reactivation from latency Pathogenesis of a model gammaherpesvirus in a natural host 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.Role of B-cell proliferation in the establishment of gammaherpesvirus latency.Murine gammaherpesvirus-68 glycoprotein B presents a difficult neutralization target to monoclonal antibodies derived from infected mice In vivo imaging of murid herpesvirus-4 infection.Murine gammaherpesvirus 68 LANA is essential for virus reactivation from splenocytes but not long-term carriage of viral genome.The murine gammaherpesvirus immediate-early Rta synergizes with IRF4, targeting expression of the viral M1 superantigen to plasma cells Viral latency and its regulation: lessons from the gamma-herpesviruses.Identification of spliced gammaherpesvirus 68 LANA and v-cyclin transcripts and analysis of their expression in vivo during latent infection Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.Infection of dendritic cells by a gamma2-herpesvirus induces functional modulation Protective antigen-independent CD8 T cell memory is maintained during {gamma}-herpesvirus persistence Activation of Vav by the gammaherpesvirus M2 protein contributes to the establishment of viral latency in B lymphocytes Illumination of murine gammaherpesvirus-68 cycle reveals a sexual transmission route from females to males in laboratory mice.Chemokine binding protein M3 of murine gammaherpesvirus 68 modulates the host response to infection in a natural host Early establishment of gamma-herpesvirus latency: implications for immune control.

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Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cells

http://www.wikidata.org/entity/Q36371017

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2002 nî lūn-bûn

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David L Woodland

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Emilio Flaño

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In-Jeong Kim

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Marcia A Blackman

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P2860

Complete sequence and genomic analysis of murine gammaherpesvirus 68

Natural history of murine -herpesvirus infection

A broad spectrum secreted chemokine binding protein encoded by a herpesvirus

Three distinct regions of the murine gammaherpesvirus 68 genome are transcriptionally active in latently infected mice.

Consideration of host-viral interactions in the pathogenesis of Kaposi's sarcoma.

Unraveling immunity to gamma-herpesviruses: a new model for understanding the role of immunity in chronic virus infection.

A model for persistent infection with Epstein-Barr virus: the stealth virus of human B cells.

Dissecting the host response to a gamma-herpesvirus.

Disruption of the murine gammaherpesvirus 68 M1 open reading frame leads to enhanced reactivation from latency.

Characterization of gammaherpesvirus 68 gene 50 transcription

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196

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12438427

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