Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
about
Gammaherpesviruses and pulmonary fibrosis: evidence from humans, horses, and rodentsT cell memory in the context of persistent herpes viral infectionsCellular mechanisms of tissue fibrosis. 7. New insights into the cellular mechanisms of pulmonary fibrosisPhosphoproteomic analyses reveal signaling pathways that facilitate lytic gammaherpesvirus replicationNatural history of murine -herpesvirus infectionIgG Fc Receptors Provide an Alternative Infection Route for Murine Gamma-Herpesvirus-68Viruses as co-factors for the initiation or exacerbation of lung fibrosisMurine gammaherpesvirus 68 encoding open reading frame 11 targets TANK binding kinase 1 to negatively regulate the host type I interferon responseVirus reconstituted from infectious bacterial artificial chromosome (BAC)-cloned murine gammaherpesvirus 68 acquires wild-type properties in vivo only after excision of BAC vector sequences.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 MHV68 M2 protein drives IL-10 dependent B cell proliferation and differentiationEndothelial cells support persistent gammaherpesvirus 68 infection.Gammaherpesvirus latency induces antibody-associated thrombocytopenia in mice.RTA promoter demethylation and histone acetylation regulation of murine gammaherpesvirus 68 reactivationPerturbation of lytic and latent gammaherpesvirus infection in the absence of the inhibitory receptor CEACAM1Viral Bcl-2-mediated evasion of autophagy aids chronic infection of gammaherpesvirus 68CD8+ T cell evasion mandates CD4+ T cell control of chronic gamma-herpesvirus infection.Virus-specific CD8(+) T cell numbers are maintained during gamma-herpesvirus reactivation in CD4-deficient mice.An in vitro system for studying murid herpesvirus-4 latency and reactivation.Quantitative analysis of the acute and long-term CD4(+) T-cell response to a persistent gammaherpesvirusInduction of protective immunity against murine gammaherpesvirus 68 infection in the absence of viral latency.Murine gammaherpesvirus 68 encodes a functional regulator of complement activationThree distinct regions of the murine gammaherpesvirus 68 genome are transcriptionally active in latently infected mice.Two kinetic patterns of epitope-specific CD8 T-cell responses following murine gammaherpesvirus 68 infection.Pathogenesis of a model gammaherpesvirus in a natural hostDissecting the host response to a gamma-herpesvirus.The murine gammaherpesvirus 68 M2 gene is required for efficient reactivation from latently infected B cells.Protein kinase C theta is not essential for T-cell-mediated clearance of murine gammaherpesvirus 68.Disruption of the murine gammaherpesvirus 68 M1 open reading frame leads to enhanced reactivation from latency.Lymphotoxin-alpha-deficient mice can clear a productive infection with murine gammaherpesvirus 68 but fail to develop splenomegaly or lymphocytosis.Murine gammaherpesvirus 68 cyclin D homologue is required for efficient reactivation from latency.T-cell vaccination alters the course of murine herpesvirus 68 infection and the establishment of viral latency in mice.Establishment and maintenance of long-term murine gammaherpesvirus 68 latency in B cells in the absence of CD40.Virus-specific and bystander CD8+ T-cell proliferation in the acute and persistent phases of a gammaherpesvirus infection.Kinetics of murine gammaherpesvirus 68 gene expression following infection of murine cells in culture and in mice.Role of CXCR3 in the immune response to murine gammaherpesvirus 68.Characterization of a novel wood mouse virus related to murid herpesvirus 4.Identification of viral genes essential for replication of murine gamma-herpesvirus 68 using signature-tagged mutagenesis.γ-Herpes virus-68, but not Pseudomonas aeruginosa or influenza A (H1N1), exacerbates established murine lung fibrosis
P2860
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P2860
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh
1998年學術文章
@zh-hant
name
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@ast
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@en
type
label
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@ast
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@en
prefLabel
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@ast
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@en
P2093
P2860
P356
P1476
Lung epithelial cells are a major site of murine gammaherpesvirus persistence.
@en
P2093
P2860
P304
P356
10.1084/JEM.187.12.1941
P407
P577
1998-06-01T00:00:00Z