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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

http://www.wikidata.org/entity/Q34345831

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Blocking antibody access to neutralizing domains on glycoproteins involved in entry as a novel mechanism of immune evasion by herpes simplex virus type 1 glycoproteins C and E Macrophages and cytokines in the early defence against herpes simplex virus Replication-Competent Viruses as Cancer Immunotherapeutics: Emerging Clinical Data IgG Fc Receptors Provide an Alternative Infection Route for Murine Gamma-Herpesvirus-68 Complement and its role in protection and pathogenesis of flavivirus infections Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses Further analysis of Marek's disease virus horizontal transmission confirms that U(L)44 (gC) and U(L)13 protein kinase activity are essential, while U(S)2 is nonessential.The extracellular domain of herpes simplex virus gE is indispensable for efficient cell-to-cell spread: evidence for gE/gI receptors Complement and viral pathogenesis Herpes simplex virus type 1 and 2 glycoprotein C prevents complement-mediated neutralization induced by natural immunoglobulin M antibody.The herpes simplex virus 1 IgG fc receptor blocks antibody-mediated complement activation and antibody-dependent cellular cytotoxicity in vivo.Resistance of mRNA translation to acute endoplasmic reticulum stress-inducing agents in herpes simplex virus type 1-infected cells requires multiple virus-encoded functions.Evasion of early antiviral responses by herpes simplex viruses.Virulence genes in herpes simplex virus type 1 corneal infection.HSV trafficking and development of gene therapy vectors with applications in the nervous system.Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.Dancing with the enemy: the interplay of herpes simplex virus with dendritic cells.Immune evasion by herpes simplex virus type 1, strategies for virus survival Complement Opsonization Promotes Herpes Simplex Virus 2 Infection of Human Dendritic Cells.HSV-1 exploits the innate immune scavenger receptor MARCO to enhance epithelial adsorption and infection.Immunization strategies to block the herpes simplex virus type 1 immunoglobulin G Fc receptor.Development and pathogenic evaluation of recombinant herpes simplex virus type 1 expressing two fluorescent reporter genes from different lytic promoters Blocking immune evasion as a novel approach for prevention and treatment of herpes simplex virus infection Immunization with HSV-1 glycoprotein C prevents immune evasion from complement and enhances the efficacy of an HSV-1 glycoprotein D subunit vaccine Herpes simplex virus as a tool to define the role of complement in the immune response to peripheral infection.Rapid host immune response and viral dynamics in herpes simplex virus-2 infection.Improving immunogenicity and efficacy of vaccines for genital herpes containing herpes simplex virus glycoprotein D.Identification of GAS-dependent interferon-sensitive target genes whose transcription is STAT2-dependent but ISGF3-independent.Differential transcription patterns in wild-type and glycoprotein G-deleted infectious laryngotracheitis viruses.Let's Tie the Knot: Marriage of Complement and Adaptive Immunity in Pathogen Evasion, for Better or Worse.Widely Used Herpes Simplex Virus 1 ICP0 Deletion Mutant Strain dl1403 and Its Derivative Viruses Do Not Express Glycoprotein C Due to a Secondary Mutation in the gC Gene Viral-derived complement inhibitors: current status and potential role in immunomodulation.Interindividual Spread of Herpesviruses.Quantitative analysis of herpes simplex virus reactivation in vivo demonstrates that reactivation in the nervous system is not inhibited at early times postinoculation Cell surface expression of the vaccinia virus complement control protein is mediated by interaction with the viral A56 protein and protects infected cells from complement attack.Characterization of the complement inhibitory function of rhesus rhadinovirus complement control protein (RCP).Glycoprotein C of herpes simplex virus type 1 is required to cause keratitis at low infectious doses in intact rabbit corneas.Identification and characterization of duck plague virus glycoprotein C gene and gene product.Mannan-binding lectin modulates the response to HSV-2 infection.Targeting human glioma cells using HSV-1 amplicon peptide display vector.

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

http://www.wikidata.org/entity/Q34345831

description

2002 nî lūn-bûn

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2002 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2002 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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type

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

@en

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

@nl

prefLabel

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

@en

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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JVI.76.18.9232-9241.2002

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Journal of Virology

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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P2093

Chad Sarver

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Dimitrios Mastellos

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Gary H Cohen

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Harvey M Friedman

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John M Lubinski

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Ming Jiang

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Yueh Chang

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P2860

gp13 (EHV-gC): a complement receptor induced by equine herpesviruses

New developments in the epidemiology, natural history and management of genital herpes.

Murine gammaherpesvirus 68 encodes a functional regulator of complement activation

In vivo immune evasion mediated by the herpes simplex virus type 1 immunoglobulin G Fc receptor.

The herpes simplex virus gE-gI complex facilitates cell-to-cell spread and binds to components of cell junctions

Herpes simplex virus type 1 glycoprotein E domains involved in virus spread and disease

Human cytomegalovirus open reading frame TRL11/IRL11 encodes an immunoglobulin G Fc-binding protein

Neutrophil priming by cytokines and vitamin D binding protein (Gc-globulin): impact on C5a-mediated chemotaxis, degranulation and respiratory burst.

Cytoplasmic domain of herpes simplex virus gE causes accumulation in the trans-Golgi network, a site of virus envelopment and sorting of virions to cell junctions.

The acquisition of herpes simplex virus during pregnancy.

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9232-9241

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10.1128/JVI.76.18.9232-9241.2002

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18

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76

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Roselyn J. Eisenberg

John D. Lambris

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2002-09-01T00:00:00Z

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12186907

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