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

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

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

http://www.wikidata.org/entity/Q35601591

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Natural history of murine -herpesvirus infection IgG Fc Receptors Provide an Alternative Infection Route for Murine Gamma-Herpesvirus-68 Subsisting H1N1 influenza memory responses are insufficient to protect from pandemic H1N1 influenza challenge in C57BL/6 mice.The murine gammaherpesvirus-68 gp150 acts as an immunogenic decoy to limit virion neutralization Post-exposure vaccination improves gammaherpesvirus neutralization Induction of protective immunity against murine gammaherpesvirus 68 infection in the absence of viral latency.The murine gammaherpesvirus 68 ORF27 gene product contributes to intercellular viral spread A persistent virus vector confers superior anti-tumor immunity, compared with a non-persistent vector.Dissecting the host response to a gamma-herpesvirus.Disruption of the murine gammaherpesvirus 68 M1 open reading frame leads to enhanced reactivation from latency.Profound protection against respiratory challenge with a lethal H7N7 influenza A virus by increasing the magnitude of CD8(+) T-cell memory Virus-specific and bystander CD8+ T-cell proliferation in the acute and persistent phases of a gammaherpesvirus infection.In vivo imaging of murid herpesvirus-4 infection.Murid herpesvirus-4 lacking thymidine kinase reveals route-dependent requirements for host colonization.In vivo importance of heparan sulfate-binding glycoproteins for murid herpesvirus-4 infection.Dendritic cells loaded with tumor B cells elicit broad immunity against murine gammaherpesvirus 68 but fail to prevent long-term latency Quantitative analysis of the CD8+ T-cell response to readily eliminated and persistent viruses Control of memory CD8+ T cell differentiation by CD80/CD86-CD28 costimulation and restoration by IL-2 during the recall response.Epstein-Barr virus IL-10 gene expression by a recombinant murine gammaherpesvirus in vivo enhances acute pathogenicity but does not affect latency or reactivation.Murine gammaherpesvirus 68 lacking thymidine kinase shows severe attenuation of lytic cycle replication in vivo but still establishes latency Glycogen Synthase Kinase 3 Inactivation Drives T-bet-Mediated Downregulation of Co-receptor PD-1 to Enhance CD8(+) Cytolytic T Cell Responses.Vaccination with murid herpesvirus-4 glycoprotein B reduces viral lytic replication but does not induce detectable virion neutralization Early establishment of gamma-herpesvirus latency: implications for immune control.Maintenance of gammaherpesvirus latency requires viral cyclin in the absence of B lymphocytes.CD80 and CD86 control antiviral CD8+ T-cell function and immune surveillance of murine gammaherpesvirus 68.Postexposure vaccination massively increases the prevalence of gamma-herpesvirus-specific CD8+ T cells but confers minimal survival advantage on CD4-deficient mice.Quantitative analysis of long-term virus-specific CD8+-T-cell memory in mice challenged with unrelated pathogens Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infection Severe gammaherpesvirus-induced pneumonitis and fibrosis in syngeneic bone marrow transplant mice is related to effects of transforming growth factor-β.CD8+ T cell dysfunction and increase in murine gammaherpesvirus latent viral burden in the absence of 4-1BB ligand Importance of antibody in virus infection and vaccine-mediated protection by a latency-deficient recombinant murine γ-herpesvirus-68 CD8+ T Cell Response to Gammaherpesvirus Infection Mediates Inflammation and Fibrosis in Interferon Gamma Receptor-Deficient Mice Tiled microarray identification of novel viral transcript structures and distinct transcriptional profiles during two modes of productive murine gammaherpesvirus 68 infection.Multiple Lytic Origins of Replication Are Required for Optimal Gammaherpesvirus Fitness In Vitro and In Vivo Antibody evasion by the N terminus of murid herpesvirus-4 glycoprotein B.Control of gammaherpesvirus latency by latent antigen-specific CD8(+) T cells.A secreted chemokine binding protein encoded by murine gammaherpesvirus-68 is necessary for the establishment of a normal latent load.Influenza and the challenge for immunology.The limits of protection by "memory" T cells in Ig-/- mice persistently infected with a gamma-herpesvirus Understanding the mechanisms and limitations of immune control of HIV.

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

http://www.wikidata.org/entity/Q35601591

description

1999 nî lūn-bûn

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1999年の論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年论文

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name

A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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Proceedings of the National Academy of Sciences of the United States of America

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A gamma-herpesvirus sneaks thr ...... rimed to a lytic-phase epitope

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G T Belz

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J D Altman

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M R Castrucci

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P G Stevenson

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P2860

Relation of Burkitt's tumor-associated herpes-ytpe virus to infectious mononucleosis

Complete sequence and genomic analysis of murine gammaherpesvirus 68

Antigen processing in vivo and the elicitation of primary CTL responses

Introduction of site-specific mutations into the genome of influenza virus

Virus-specific CD8(+) T cell numbers are maintained during gamma-herpesvirus reactivation in CD4-deficient mice.

Quantitative analysis of the acute and long-term CD4(+) T-cell response to a persistent gammaherpesvirus

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

Diversity of T-cell receptors in virus-specific cytotoxic T lymphocytes recognizing three distinct viral epitopes restricted by a single major histocompatibility complex molecule.

Minimal epitopes expressed in a recombinant polyepitope protein are processed and presented to CD8+ cytotoxic T cells: implications for vaccine design.

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

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9281-9286

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scholarly article

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10.1073/PNAS.96.16.9281

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16

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96

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Peter C. Doherty

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1999-08-01T00:00:00Z

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12868688

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10430934

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17771

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