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1 EHV-1 and BHV-1 Us9 were able to fully compensate for th
2 EHV-1 entry was thought to occur exclusively through fus
3 EHV-1 productively infected four of these cell lines, an
4 EHV-1 strain KyA is attenuated in the mouse and equine,
5 EHV-1-specific CTL could be restimulated from the spleen
7 h the alphaherpesvirus equine herpesvirus 1 (EHV-1) displayed reduced body weight loss but had higher
8 t the alphaherpesvirus equine herpesvirus 1 (EHV-1) efficiently entered and replicated in CHO-K1 cell
9 placed with the SRT of equine herpesvirus 1 (EHV-1) IEP, its trans-activation activity was completely
13 best option to combat equine herpesvirus 1 (EHV-1) infection, and several different strategies of va
16 2 protein (EICP22P) of Equine herpesvirus 1 (EHV-1) is an early protein that functions synergisticall
17 The EICP0 protein of equine herpesvirus 1 (EHV-1) is an early, viral regulatory protein that indepe
18 tivates all classes of equine herpesvirus 1 (EHV-1) promoters but, unexpectedly, trans-activates its
19 iently transduced with equine herpesvirus 1 (EHV-1) reconstituted from viral DNA maintained and manip
20 lung by the pathogenic equine herpesvirus 1 (EHV-1) strain RacL11 in comparison to infection with the
23 rus type 1 (HSV-1) and equine herpesvirus 1 (EHV-1), and of channel catfish virus, an evolutionarily
24 er alphaherpesviruses: equine herpesvirus 1 (EHV-1), varicella-zoster virus, and pseudorabies virus,
27 rinary pathogens, equine herpesvirus type 1 (EHV-1) and bovine herpesvirus type 1 (BHV-1), and fused
28 (DI) particles of equine herpesvirus type 1 (EHV-1) are capable of mediating persistent infection.
29 Here, we used equine herpesvirus type 1 (EHV-1) as a model to determine residues in EHV-1 gG that
30 is study, we used equine herpesvirus type 1 (EHV-1) as a model to study the pathophysiological import
32 s the role of the equine herpesvirus type 1 (EHV-1) ICP0 protein (EICP0) in gene regulation, a variet
33 ytic animal virus equine herpesvirus type 1 (EHV-1) was evaluated for its oncolytic potential against
35 s type 1 (BHV-1), equine herpesvirus type 1 (EHV-1), pseudorabies virus (PRV), and varicella-zoster v
38 howed that the EICP0 protein trans-activated EHV-1 promoters harboring only a minimal promoter region
39 y protein that independently trans-activates EHV-1 immediate-early (IE), early, gamma1 late, and gamm
40 sting that the EICP0 protein trans-activates EHV-1 promoters by interactions with general transcripti
44 binant virus was constructed by inserting an EHV-1 gD expression cassette under the control of the cy
45 oma cells, these cells were infected with an EHV-1 lacZ reporter virus, and cells that supported viru
47 together to significantly trans-activate any EHV-1 promoter, and (iv) the EICP27 and EICP0 proteins f
48 e, this is the first report of an attenuated EHV-1 vaccine that protects the animal at 1 to 7 days po
49 t EHV-1 KyA may be used as a live attenuated EHV-1 vaccine as well as a prophylactic agent in horses.
50 .n.) inoculation of mice with the attenuated EHV-1 strain KyA resulted in the generation of a primary
55 protein; and (iv) the EICP0 protein of both EHV-1 strains is a potent transactivator of EHV-1 genes.
57 ed that (i) the IR2P by itself downregulated EHV-1 early promoters (EICP0, TK, EICP22, and EICP27) in
58 As with other alphaherpesviruses, efficient EHV-1 entry was dependent on glycoprotein D and cell sur
61 ough this rPCR assay can detect and genotype EHV-1 strains, subsequent studies demonstrated that it l
64 entation assays showed that the TAD of IE62, EHV-1 IEP, and HSV-1 VP16 interacted with Mediator 25 in
65 ected cells; however, the amount of NREBP in EHV-1-infected L-M cells that bound to the Nb oligonucle
66 rapid early host protein shutoff occurred in EHV-1-infected cells led us to test EHV-1 vhs activity m
68 (EHV-1) as a model to determine residues in EHV-1 gG that are involved in the processes of chemokine
70 V-1-susceptible cell type were inserted into EHV-1-resistant B78H1 murine melanoma cells, these cells
72 acrophages and protected mice against lethal EHV-1 challenge, suggesting that IFN-gamma expression is
75 r was absolutely essential for activation of EHV-1 promoters, since deletion of the entire RING finge
76 ICP0 proteins are potent trans-activators of EHV-1 promoters; however, in transient-transfection assa
79 f representative promoters of all classes of EHV-1 genes and contains a negative regulatory element (
80 sufficient for activation of all classes of EHV-1 promoters, (iii) the RING finger was absolutely es
81 sential function in the replication cycle of EHV-1, and its main role appears to be in secondary enve
85 a vector for the heterologous expression of EHV-1 glycoprotein D (gD) and that the intramuscular imm
87 or the detection and A/G(2254) genotyping of EHV-1, making this improved rPCR assay a valuable diagno
88 , comprehensive analysis of glycosylation of EHV-1 gG revealed that N-glycosylation is not required f
90 antly, in vivo analyses in a murine model of EHV-1 infection showed that neutrophil migration in the
91 The NREBP is also present in the nucleus of EHV-1-infected cells; however, the amount of NREBP in EH
93 of ORF30 was used to confirm the presence of EHV-1 and characterize the genotype (A(2254) or G(2254))
94 d glycoproteins the hypervariable regions of EHV-1 gG, a vCKBP, and the closely related EHV-4 gG, whi
100 When inserted into the promoters of other EHV-1 genes, this sequence also downregulated activation
101 or functions in conjunction with three other EHV-1 regulatory proteins to activate expression of the
102 in that functions synergistically with other EHV-1 regulatory proteins to transactivate the expressio
103 nalysis revealed that EUs4 of the pathogenic EHV-1 strain RacL11 is an open reading frame of 2,376 bp
106 on and virus growth assays, the IR2P reduced EHV-1 production by 23-fold compared to virus titers ach
109 urred in EHV-1-infected cells led us to test EHV-1 vhs activity more thoroughly and to examine the ex
112 the data in this study provide evidence that EHV-1 entry via endocytosis is triggered by the interact
113 RSD motif present in gD and, moreover, that EHV-1 uses different cellular entry pathways to infect i
118 aveola-dependent endocytosis, we showed that EHV-1 entry into CHO-K1 cells does not require clathrin
121 , and its broad tissue tropism suggests that EHV-1 may use multiple receptors to initiate virus entry
122 mary, we demonstrate for the first time that EHV-1 gG not only binds to chemokines but is also capabl
125 ever, further analyses revealed that (i) the EHV-1 vhs homolog gene, ORF19, was transcribed and trans
126 l analysis revealed that an RSD motif in the EHV-1 envelope glycoprotein D (gD) is critical for entry
131 detected in cells infected with any of three EHV-1 strains (Ab4, KyA, and KyD) at multiplicities of i
132 etermine the relative contribution of gp2 to EHV-1 pathogenesis, we compared the course of respirator
134 s we conclude that full-length and truncated EHV-1 gp2 are not functionally equivalent and cannot com
138 s demonstrated that vaccination with the VC2-EHV-1-gD vaccine stimulated robust IgG1 and IgG2a antibo
139 nimals.IMPORTANCE A novel virus-vectored VC2-EHV-1-gD vaccine was constructed using the live-attenuat
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