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1 BHV-1 DNA was consistently detected in the tonsils of la
2 BHV-1 is a major viral pathogen of Bovine Respiratory Di
3 BHV-1.1 is a respiratory pathogen of highly restricted h
5 l protein 0 encoded by bovine herpesvirus 1 (BHV-1) (bICP0) is necessary for efficient productive inf
6 latently infected with bovine herpesvirus 1 (BHV-1) abundantly express latency-related (LR) RNA (LR-R
7 orabies virus (PRV) or bovine herpesvirus 1 (BHV-1) entry, did not reduce homotypic trans interaction
11 uring acute infection, bovine herpesvirus 1 (BHV-1) gene expression is extinguished, many neurons sur
12 of nonneuronal cells, bovine herpesvirus 1 (BHV-1) gene expression proceeds in a well-defined cascad
13 orms, and oligomers of bovine herpesvirus 1 (BHV-1) gI and gE proteins with polyvalent rabbit serum s
17 g acute infection, the bovine herpesvirus 1 (BHV-1) infection cycle is blocked in sensory ganglionic
23 ed transcript (LRT) of bovine herpesvirus 1 (BHV-1) is the only abundant viral RNA detected during la
25 fficiently express the bovine herpesvirus 1 (BHV-1) membrane proteins gI and gE at the PRV gG locus.
26 fection of cattle with bovine herpesvirus 1 (BHV-1) represses cell-mediated immunity, which can lead
27 fection of calves with bovine herpesvirus 1 (BHV-1) results in transient immunosuppression that may l
30 ssion vectors carrying bovine herpesvirus 1 (BHV-1) VP22 (BVP22) or herpes simplex virus type 1 (HSV-
31 SV-1 VP22 (HVP22) with bovine herpesvirus 1 (BHV-1) VP22 (BVP22) using green fluorescent protein (GFP
40 ype 1 (EHV-1) and bovine herpesvirus type 1 (BHV-1), and fused them to enhanced green fluorescent pro
41 ated proteins of bovine herpes virus type 1 (BHV-1), equine herpesvirus type 1 (EHV-1), pseudorabies
42 and its homolog from bovine herpes-virus 1 (BHV-1) can each recruit the human homeodomain protein Oc
43 n mucosal epithelium, bovine herpes virus 1 (BHV-1) establishes lifelong latency in sensory neurons w
45 ng the model pathogen Bovine Herpes Virus-1 (BHV-1) this study employs an extended-gate field-effect
48 surface to serve as a capture antigen for a BHV-1-specific antibody (anti-gE), produced in cattle in
51 pecifically with antibodies prepared against BHV-1 U(L)49.5, previously reported to be a 9-kDa protei
58 ructural requirements for HSV entry, PRV and BHV-1 entry, and homotypic and heterotypic trans interac
59 ns of nectin-2 impaired the entry of PRV and BHV-1 when introduced into either nectin-1 or nectin-2,
61 ti-gE present in commercially available anti-BHV-1 antiserum and in real serum samples from cattle wi
64 but not CD8(+) lymphocytes were infected by BHV-1 as judged by in situ hybridization and PCR, respec
66 esis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gED
71 leted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressing BHV-5 gE (BHV-
73 n U(L)3.5 and alphaBTIF may be important for BHV-1 maturation and regulation of alphaBTIF transactiva
74 After acute infection, the primary site for BHV-1 latency is sensory neurons in the trigeminal gangl
77 on mass spectrometry analysis, we identified BHV-1 alpha-transinducing factor (alphaBTIF) as a BHV-1
81 fraction of pulse-labeled gI synthesized in BHV-1-infected cells apparently is cleaved into two rela
90 We examined the induction and activity of BHV-1-specific cytolytic CD4(+) T lymphocytes (CTL) by s
97 gE in the differential neuropathogenesis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 rec
99 mportant role in the latency/pathogenesis of BHV-1, construction of a mutant is necessary to test thi
103 ent of the predicted amino acid sequences of BHV-1 and BHV-5 gE open reading frames showed that they
105 geminal ganglia (TG) are the primary site of BHV-1 latency, viral genomes are detected in the tonsils
106 Our experiments used the Colorado strain of BHV-1 and mutant viruses with insertions of the Escheric
107 ed (LR) region departs markedly from that of BHV-1 in both coding and transcriptional regulatory regi
108 reover, the binding sites for HSV and PRV or BHV-1 gDs on nectin-1 may overlap but are not identical.
110 that observed after infection with parental BHV-1, and there were no observable differences in proce
115 Taken together, these results indicate that BHV-1 can infect CD4(+) T cells in cattle, leading to ap
118 rom the HSV-1 VP16 response element, and the BHV-1 VP16 protein activates transcription from the BHV-
123 d CJLAT, contains two complete copies of the BHV-1 LR gene (one in each viral long repeat) in place o
126 gly, in a portion of the animals tested, the BHV-1.1 gE and gI proteins functioned autonomously to pr
127 ation resulting from this report is that the BHV-1 gE and gI proteins functioned together to compleme
133 he sensor capabilities as a diagnostic tool, BHV-1 viral protein gE was expressed and immobilized on
135 t seizure model that distinguished wild-type BHV-1 and -5 based on their differential neuropathogenes
137 omosome containing a wild-type (wt) virulent BHV-1 strain to generate a single amino acid mutation in
138 udorabies virus, and varicella-zoster virus, BHV-1 gI and gE are modified by N-linked glycosylation a
142 infection of bovine kidney (MDBK) cells with BHV-1 leads to PCD, as judged by terminal deoxynucleotid
148 that CD4(+) CTL lyse macrophages pulsed with BHV-1 polypeptides through a Fas-mediated lytic pathway
152 ith the LR mutant to calves infected with wt BHV-1 because LR gene products inhibit apoptosis in tran
153 ntrast, all calves latently infected with wt BHV-1 or the LR rescued mutant reactivate from latency a
154 reatment of calves latently infected with wt BHV-1 or the LR-rescued virus, but not the LR mutant, co
157 we compared the abilities of wild-type (wt) BHV-1 and a strain with a mutation in the LR gene (the L
158 calves latently infected with wild-type (wt) BHV-1 or the LR rescued virus, the LR mutant virus does
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