Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infection - Wikidata - wikimedia - TriplyDB

Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infection

Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infection

http://www.wikidata.org/entity/Q35149326

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A virtual look at Epstein-Barr virus infection: biological interpretations Murid herpesvirus-4 exploits dendritic cells to infect B cells Murine gamma-herpesvirus 68 hijacks MAVS and IKKbeta to initiate lytic replication Latent gammaherpesvirus 68 infection induces distinct transcriptional changes in different organs 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.Identification of closely spaced but distinct transcription initiation sites for the murine gammaherpesvirus 68 latency-associated M2 gene.The Murid Herpesvirus-4 gL regulates an entry-associated conformation change in gH.A single CD8+ T cell epitope sets the long-term latent load of a murid herpesvirus Perturbation of lytic and latent gammaherpesvirus infection in the absence of the inhibitory receptor CEACAM1 Ex vivo stimulation of B cells latently infected with gammaherpesvirus 68 triggers reactivation from latency 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.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.A gammaherpesvirus cooperates with interferon-alpha/beta-induced IRF2 to halt viral replication, control reactivation, and minimize host lethality.Murine gammaherpesvirus 68 infection is associated with lymphoproliferative disease and lymphoma in BALB beta2 microglobulin-deficient mice A gammaherpesvirus 68 gene 50 null mutant establishes long-term latency in the lung but fails to vaccinate against a wild-type virus challenge.Myeloid infection links epithelial and B cell tropisms of Murid Herpesvirus-4.Protective antigen-independent CD8 T cell memory is maintained during {gamma}-herpesvirus persistence Early establishment of gamma-herpesvirus latency: implications for immune control.Type I interferons link viral infection to enhanced epithelial turnover and repair.Evidence for CDK-dependent and CDK-independent functions of the murine gammaherpesvirus 68 v-cyclin.Rhadinovirus host entry by co-operative infection.Recombinant Murine Gamma Herpesvirus 68 Carrying KSHV G Protein-Coupled Receptor Induces Angiogenic Lesions in Mice Importance of antibody in virus infection and vaccine-mediated protection by a latency-deficient recombinant murine γ-herpesvirus-68 Multiple Lytic Origins of Replication Are Required for Optimal Gammaherpesvirus Fitness In Vitro and In Vivo Murine gammaherpesvirus-68 expands, but does not activate, CD11b+ gr-1+ splenocytes in vivo Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation from Latency by Preventing Virus-Induced Systemic Inflammation.The limits of protection by "memory" T cells in Ig-/- mice persistently infected with a gamma-herpesvirus The absence of M1 leads to increased establishment of murine gammaherpesvirus 68 latency in IgD-negative B cells.Murine Gammaherpesvirus 68 LANA and SOX Homologs Counteract ATM-Driven p53 Activity during Lytic Viral Replication Sleep and fatigue in mice infected with murine gammaherpesvirus 68.Targeting the nuclear antigen 1 of Epstein-Barr virus to the human endocytic receptor DEC-205 stimulates protective T-cell responses.Gammaherpesvirus modulation of mouse adenovirus type 1 pathogenesis The CD8 T-cell response against murine gammaherpesvirus 68 is directed toward a broad repertoire of epitopes from both early and late antigens.Suppression of TLR9 immunostimulatory motifs in the genome of a gammaherpesvirus Glycoprotein B cleavage is important for murid herpesvirus 4 to infect myeloid cells

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Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infection

http://www.wikidata.org/entity/Q35149326

description

2003 nî lūn-bûn

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2003 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2003 թվականի հուլիսին հրատարակված գիտական հոդված

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2003年の論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年论文

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Establishment and maintenance ...... ve dose and route of infection

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Establishment and maintenance ...... ve dose and route of infection

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Establishment and maintenance ...... ve dose and route of infection

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Establishment and maintenance ...... ve dose and route of infection

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Establishment and maintenance ...... ve dose and route of infection

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Establishment and maintenance ...... ve dose and route of infection

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JVI.77.13.7696-7701.2003

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Journal of Virology

P1476

Establishment and maintenance ...... ve dose and route of infection

@en

P2093

James S McClellan

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Joy Loh

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Meagan A Jacoby

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Samuel H Speck

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Scott A Tibbetts

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Sharookh B Kapadia

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Victor Van Berkel

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P2860

The probability of in vivo reactivation of herpes simplex virus type 1 increases with the number of latently infected neurons in the ganglia.

Mucosal and parenteral vaccination against acute and latent murine cytomegalovirus (MCMV) infection by using an attenuated MCMV mutant.

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

Optimized viral dose and transient immunosuppression enable herpes simplex virus ICP0-null mutants To establish wild-type levels of latency in vivo.

T-cell vaccination alters the course of murine herpesvirus 68 infection and the establishment of viral latency in mice.

Disruption of the M2 gene of murine gammaherpesvirus 68 alters splenic latency following intranasal, but not intraperitoneal, inoculation.

A gamma-herpesvirus sneaks through a CD8(+) T cell response primed to a lytic-phase epitope

Comprehensive quantification of herpes simplex virus latency at the single-cell level

CD4(+) T cell-mediated control of a gamma-herpesvirus in B cell-deficient mice is mediated by IFN-gamma.

Progressive loss of CD8+ T cell-mediated control of a gamma-herpesvirus in the absence of CD4+ T cells.

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7696-7701

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scholarly article

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10.1128/JVI.77.13.7696-7701.2003

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13

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77

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Herbert W. "Skip" Virgin

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2003-07-01T00:00:00Z

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10710188

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12805472

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164792

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