Herpes simplex virus type 1 evades the effects of antibody and complement in vivo
about
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 EMacrophages and cytokines in the early defence against herpes simplex virusReplication-Competent Viruses as Cancer Immunotherapeutics: Emerging Clinical DataIgG Fc Receptors Provide an Alternative Infection Route for Murine Gamma-Herpesvirus-68Complement and its role in protection and pathogenesis of flavivirus infectionsInterleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responsesFurther 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 receptorsComplement and viral pathogenesisHerpes 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 survivalComplement 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 promotersBlocking immune evasion as a novel approach for prevention and treatment of herpes simplex virus infectionImmunization with HSV-1 glycoprotein C prevents immune evasion from complement and enhances the efficacy of an HSV-1 glycoprotein D subunit vaccineHerpes 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 GeneViral-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 postinoculationCell 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.
P2860
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P2860
Herpes simplex virus type 1 evades the effects of antibody and complement in vivo
description
2002 nî lūn-bûn
@nan
2002 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Herpes simplex virus type 1 evades the effects of antibody and complement in vivo
@ast
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
type
label
Herpes simplex virus type 1 evades the effects of antibody and complement in vivo
@ast
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
@ast
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
P2093
P2860
P50
P1433
P1476
Herpes simplex virus type 1 evades the effects of antibody and complement in vivo
@en
P2093
Chad Sarver
Dimitrios Mastellos
Gary H Cohen
Harvey M Friedman
John M Lubinski
Ming Jiang
Yueh Chang
P2860
P304
P356
10.1128/JVI.76.18.9232-9241.2002
P407
P577
2002-09-01T00:00:00Z