Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread.
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Herpes simplex virus with highly reduced gD levels can efficiently enter and spread between human keratinocytes.The soluble ectodomain of herpes simplex virus gD contains a membrane-proximal pro-fusion domain and suffices to mediate virus entryHerpes simplex virus type 1 glycoprotein e is required for axonal localization of capsid, tegument, and membrane glycoproteins.Human cytomegalovirus entry into epithelial and endothelial cells depends on genes UL128 to UL150 and occurs by endocytosis and low-pH fusion.Truncated forms of glycoprotein D of herpes simplex virus 1 capable of blocking apoptosis and of low-efficiency entry into cells form a heterodimer dependent on the presence of a cysteine located in the shared transmembrane domains.Herpes simplex virus glycoproteins gB and gD function in a redundant fashion to promote secondary envelopmentHerpes simplex virus glycoproteins gD and gE/gI serve essential but redundant functions during acquisition of the virion envelope in the cytoplasm.The epithelial αvβ3-integrin boosts the MYD88-dependent TLR2 signaling in response to viral and bacterial components.Cytoplasmic residues of herpes simplex virus glycoprotein gE required for secondary envelopment and binding of tegument proteins VP22 and UL11 to gE and gDRapid genome assembly and comparison decode intrastrain variation in human alphaherpesviruses.Glycoprotein D-independent spread of pseudorabies virus infection in cultured peripheral nervous system neurons in a compartmented system.Griffithsin protects mice from genital herpes by preventing cell-to-cell spreadDisplacement of the C terminus of herpes simplex virus gD is sufficient to expose the fusion-activating interfaces on gD.Varicella-zoster virus and herpes simplex virus 1 can infect and replicate in the same neurons whether co- or superinfected.Development of an oncolytic HSV vector fully retargeted specifically to cellular EpCAM for virus entry and cell-to-cell spread.Novel mutations in gB and gH circumvent the requirement for known gD Receptors in herpes simplex virus 1 entry and cell-to-cell spread.Insertions in the gG gene of pseudorabies virus reduce expression of the upstream Us3 protein and inhibit cell-to-cell spread of virus infection.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 recognitionHerpes simplex virus type 1 primary envelopment: UL34 protein modification and the US3-UL34 catalytic relationshipThe herpes simplex virus 1 UL51 protein interacts with the UL7 protein and plays a role in its recruitment into the virion.The virological synapse facilitates herpes simplex virus entry into T cells.Vaccine-induced antibodies to herpes simplex virus glycoprotein D epitopes involved in virus entry and cell-to-cell spread correlate with protection against genital disease in guinea pigs.
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P2860
Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread.
description
2000 nî lūn-bûn
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2000年の論文
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2000年論文
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2000年論文
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2000年論文
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2000年論文
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2000年論文
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2000年论文
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name
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@en
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@nl
type
label
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@en
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@nl
prefLabel
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@en
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@nl
P2093
P2860
P1433
P1476
Mutations in herpes simplex vi ...... e virus from cell-cell spread.
@en
P2093
N Rodriguez
R J Roller
P2860
P304
11437-11446
P356
10.1128/JVI.74.24.11437-11446.2000
P407
P577
2000-12-01T00:00:00Z