Generation of herpesvirus entry mediator (HVEM)-restricted herpes simplex virus type 1 mutant viruses: resistance of HVEM-expressing cells and identification of mutations that rescue nectin-1 recognition
about
Structure of Herpes Simplex Virus Glycoprotein D Bound to the Human Receptor Nectin-1Herpes virus fusion and entry: a story with many characters.Bispecific adapter-mediated retargeting of a receptor-restricted HSV-1 vector to CEA-bearing tumor cells.The soluble amino-terminal region of HVEM mediates efficient herpes simplex virus type 1 infection of gD receptor-negative cells.Herpesvirus entry mediator on radiation-resistant cell lineages promotes ocular herpes simplex virus 1 pathogenesis in an entry-independent manner.A herpes simplex virus 2 glycoprotein D mutant generated by bacterial artificial chromosome mutagenesis is severely impaired for infecting neuronal cells and infects only Vero cells expressing exogenous HVEM.A Herpes Simplex Virus 2 (HSV-2) gD Mutant Impaired for Neural Tropism Is Superior to an HSV-2 gD Subunit Vaccine To Protect Animals from Challenge with HSV-2.Neuroblastomas vary widely in their sensitivities to herpes simplex virotherapy unrelated to virus receptors and susceptibility.Regulation of herpes simplex virus gB-induced cell-cell fusion by mutant forms of gH/gL in the absence of gD and cellular receptors.Effective treatment of an orthotopic xenograft model of human glioblastoma using an EGFR-retargeted oncolytic herpes simplex virusOncolytic HSV virotherapy in murine sarcomas differentially triggers an antitumor T-cell response in the absence of virus permissivity.Expression of HSV-1 receptors in EBV-associated lymphoproliferative disease determines susceptibility to oncolytic HSV.Dual split protein-based fusion assay reveals that mutations to herpes simplex virus (HSV) glycoprotein gB alter the kinetics of cell-cell fusion induced by HSV entry glycoproteinsInduction of conformational changes at the N-terminus of herpes simplex virus glycoprotein D upon binding to HVEM and nectin-1HSV Recombinant Vectors for Gene Therapy.Syncytial Mutations Do Not Impair the Specificity of Entry and Spread of a Glycoprotein D Receptor-Retargeted Herpes Simplex Virus.Development of an oncolytic HSV vector fully retargeted specifically to cellular EpCAM for virus entry and cell-to-cell spread.Retargeting of herpes simplex virus (HSV) vectors.Novel mutations in gB and gH circumvent the requirement for known gD Receptors in herpes simplex virus 1 entry and cell-to-cell spread.Mechanism of HSV infection through soluble adapter-mediated virus bridging to the EGF receptor.A double mutation in glycoprotein gB compensates for ineffective gD-dependent initiation of herpes simplex virus type 1 infection.
P2860
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P2860
Generation of herpesvirus entry mediator (HVEM)-restricted herpes simplex virus type 1 mutant viruses: resistance of HVEM-expressing cells and identification of mutations that rescue nectin-1 recognition
description
2009 nî lūn-bûn
@nan
2009年の論文
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2009年学术文章
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2009年学术文章
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2009年学术文章
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2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
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2009年學術文章
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2009年學術文章
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name
Generation of herpesvirus entr ...... at rescue nectin-1 recognition
@en
Generation of herpesvirus entry mediator
@nl
type
label
Generation of herpesvirus entr ...... at rescue nectin-1 recognition
@en
Generation of herpesvirus entry mediator
@nl
prefLabel
Generation of herpesvirus entr ...... at rescue nectin-1 recognition
@en
Generation of herpesvirus entry mediator
@nl
P2093
P2860
P356
P1433
P1476
Generation of herpesvirus entr ...... at rescue nectin-1 recognition
@en
P2093
Arthur R Frampton
Hiroaki Uchida
Joseph C Glorioso
Paola Grandi
Waris A Shah
William F Goins
P2860
P304
P356
10.1128/JVI.01449-08
P407
P577
2009-01-07T00:00:00Z