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1 EHV-1 and BHV-1 Us9 were able to fully compensate for th
2 EHV-1 did not alter the cellular level of Janus-activate
3 EHV-1 entry was thought to occur exclusively through fus
4 EHV-1 is transmitted with respiratory secretions by nose
5 EHV-1 productively infected four of these cell lines, an
6 EHV-1 strain KyA is attenuated in the mouse and equine,
7 EHV-1-specific CTL could be restimulated from the spleen
9 h the alphaherpesvirus equine herpesvirus 1 (EHV-1) displayed reduced body weight loss but had higher
10 t the alphaherpesvirus equine herpesvirus 1 (EHV-1) efficiently entered and replicated in CHO-K1 cell
11 placed with the SRT of equine herpesvirus 1 (EHV-1) IEP, its trans-activation activity was completely
15 best option to combat equine herpesvirus 1 (EHV-1) infection, and several different strategies of va
19 2 protein (EICP22P) of Equine herpesvirus 1 (EHV-1) is an early protein that functions synergisticall
20 The EICP0 protein of equine herpesvirus 1 (EHV-1) is an early, viral regulatory protein that indepe
21 tivates all classes of equine herpesvirus 1 (EHV-1) promoters but, unexpectedly, trans-activates its
22 iently transduced with equine herpesvirus 1 (EHV-1) reconstituted from viral DNA maintained and manip
23 lung by the pathogenic equine herpesvirus 1 (EHV-1) strain RacL11 in comparison to infection with the
26 rus type 1 (HSV-1) and equine herpesvirus 1 (EHV-1), and of channel catfish virus, an evolutionarily
28 er alphaherpesviruses: equine herpesvirus 1 (EHV-1), varicella-zoster virus, and pseudorabies virus,
31 rinary pathogens, equine herpesvirus type 1 (EHV-1) and bovine herpesvirus type 1 (BHV-1), and fused
32 (DI) particles of equine herpesvirus type 1 (EHV-1) are capable of mediating persistent infection.
33 Here, we used equine herpesvirus type 1 (EHV-1) as a model to determine residues in EHV-1 gG that
34 is study, we used equine herpesvirus type 1 (EHV-1) as a model to study the pathophysiological import
35 t EHV-1.IMPORTANCEEquine herpesvirus type 1 (EHV-1) causes respiratory disease, abortion storms, and
37 s the role of the equine herpesvirus type 1 (EHV-1) ICP0 protein (EICP0) in gene regulation, a variet
40 .IMPORTANCE Nasal equine herpesvirus type 1 (EHV-1) shedding is essential for virus transmission duri
41 ytic animal virus equine herpesvirus type 1 (EHV-1) was evaluated for its oncolytic potential against
43 s type 1 (BHV-1), equine herpesvirus type 1 (EHV-1), pseudorabies virus (PRV), and varicella-zoster v
46 n-immune horses, together with low or absent EHV-1-specific neutralizing antibodies during viral repl
47 howed that the EICP0 protein trans-activated EHV-1 promoters harboring only a minimal promoter region
48 y protein that independently trans-activates EHV-1 immediate-early (IE), early, gamma1 late, and gamm
49 sting that the EICP0 protein trans-activates EHV-1 promoters by interactions with general transcripti
53 ic understanding of mucosal immunity against EHV-1 and can support the development of enhanced diagno
54 al replication, and mucosal immunity against EHV-1.IMPORTANCEEquine herpesvirus type 1 (EHV-1) causes
58 may constitute markers of protection against EHV-1 and be utilized as indicators for improved vaccine
60 binant virus was constructed by inserting an EHV-1 gD expression cassette under the control of the cy
62 oma cells, these cells were infected with an EHV-1 lacZ reporter virus, and cells that supported viru
63 l responses, antibody isotype functions, and EHV-1 replication of susceptible (non-immune) and clinic
65 together to significantly trans-activate any EHV-1 promoter, and (iv) the EICP27 and EICP0 proteins f
66 e, this is the first report of an attenuated EHV-1 vaccine that protects the animal at 1 to 7 days po
67 t EHV-1 KyA may be used as a live attenuated EHV-1 vaccine as well as a prophylactic agent in horses.
68 .n.) inoculation of mice with the attenuated EHV-1 strain KyA resulted in the generation of a primary
73 As characteristic alphaherpesviruses, both EHV-1 and EHV-4 can establish latency, resulting in a li
74 protein; and (iv) the EICP0 protein of both EHV-1 strains is a potent transactivator of EHV-1 genes.
77 assay (EHV1-4MP) that simultaneously detects EHV-1 and EHV-4 and includes an endogenous internal cont
79 ed that (i) the IR2P by itself downregulated EHV-1 early promoters (EICP0, TK, EICP22, and EICP27) in
80 As with other alphaherpesviruses, efficient EHV-1 entry was dependent on glycoprotein D and cell sur
83 etermined to be approximately two copies for EHV-1, four copies for EHV-4, and 10 copies for the equi
85 ough this rPCR assay can detect and genotype EHV-1 strains, subsequent studies demonstrated that it l
92 entation assays showed that the TAD of IE62, EHV-1 IEP, and HSV-1 VP16 interacted with Mediator 25 in
94 ected cells; however, the amount of NREBP in EHV-1-infected L-M cells that bound to the Nb oligonucle
95 rapid early host protein shutoff occurred in EHV-1-infected cells led us to test EHV-1 vhs activity m
97 (EHV-1) as a model to determine residues in EHV-1 gG that are involved in the processes of chemokine
99 V-1-susceptible cell type were inserted into EHV-1-resistant B78H1 murine melanoma cells, these cells
101 acrophages and protected mice against lethal EHV-1 challenge, suggesting that IFN-gamma expression is
103 mune horses secreted high amounts of mucosal EHV-1-specific IgG4/7 antibodies and quickly upregulated
104 ame 2 deletion mutant of the neuropathogenic EHV-1 strain Ab4 (Ab4DeltaORF2) was tested as a vaccine
105 eexisting nasal IgG4/7 antibodies neutralize EHV-1, prevent viral entry, and thereby protect from dis
109 r was absolutely essential for activation of EHV-1 promoters, since deletion of the entire RING finge
110 ICP0 proteins are potent trans-activators of EHV-1 promoters; however, in transient-transfection assa
113 f representative promoters of all classes of EHV-1 genes and contains a negative regulatory element (
114 sufficient for activation of all classes of EHV-1 promoters, (iii) the RING finger was absolutely es
115 sential function in the replication cycle of EHV-1, and its main role appears to be in secondary enve
121 a vector for the heterologous expression of EHV-1 glycoprotein D (gD) and that the intramuscular imm
123 or the detection and A/G(2254) genotyping of EHV-1, making this improved rPCR assay a valuable diagno
124 , comprehensive analysis of glycosylation of EHV-1 gG revealed that N-glycosylation is not required f
126 detected reference and clinical isolates of EHV-1 and EHV-4, and did not detect other equid herpesvi
128 antly, in vivo analyses in a murine model of EHV-1 infection showed that neutrophil migration in the
129 The NREBP is also present in the nucleus of EHV-1-infected cells; however, the amount of NREBP in EH
131 of ORF30 was used to confirm the presence of EHV-1 and characterize the genotype (A(2254) or G(2254))
132 d glycoproteins the hypervariable regions of EHV-1 gG, a vCKBP, and the closely related EHV-4 gG, whi
133 al antibodies can prevent the replication of EHV-1 at the epithelium of the URT and, thereby, the pro
139 When inserted into the promoters of other EHV-1 genes, this sequence also downregulated activation
140 or functions in conjunction with three other EHV-1 regulatory proteins to activate expression of the
141 in that functions synergistically with other EHV-1 regulatory proteins to transactivate the expressio
142 nalysis revealed that EUs4 of the pathogenic EHV-1 strain RacL11 is an open reading frame of 2,376 bp
146 on and virus growth assays, the IR2P reduced EHV-1 production by 23-fold compared to virus titers ach
151 was linked to preexisting local and systemic EHV-1-specific antibodies combined with rapidly increasi
152 urred in EHV-1-infected cells led us to test EHV-1 vhs activity more thoroughly and to examine the ex
155 the data in this study provide evidence that EHV-1 entry via endocytosis is triggered by the interact
156 RSD motif present in gD and, moreover, that EHV-1 uses different cellular entry pathways to infect i
162 aveola-dependent endocytosis, we showed that EHV-1 entry into CHO-K1 cells does not require clathrin
165 , and its broad tissue tropism suggests that EHV-1 may use multiple receptors to initiate virus entry
166 mary, we demonstrate for the first time that EHV-1 gG not only binds to chemokines but is also capabl
170 ever, further analyses revealed that (i) the EHV-1 vhs homolog gene, ORF19, was transcribed and trans
171 l analysis revealed that an RSD motif in the EHV-1 envelope glycoprotein D (gD) is critical for entry
176 detected in cells infected with any of three EHV-1 strains (Ab4, KyA, and KyD) at multiplicities of i
177 etermine the relative contribution of gp2 to EHV-1 pathogenesis, we compared the course of respirator
179 s we conclude that full-length and truncated EHV-1 gp2 are not functionally equivalent and cannot com
180 and IgG4/7 and rapid B-cell activation upon EHV-1 infection are essential for virus neutralization,
184 s demonstrated that vaccination with the VC2-EHV-1-gD vaccine stimulated robust IgG1 and IgG2a antibo
185 nimals.IMPORTANCE A novel virus-vectored VC2-EHV-1-gD vaccine was constructed using the live-attenuat