ライフサイエンスコーパス: BHV-1

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

4 homologs, is called bovine herpesvirus 1.1 (BHV-1.1).

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

8 Bovine herpesvirus 1 (BHV-1) establishes a latent infection in the sensory gan

9 Bovine herpesvirus 1 (BHV-1) establishes a lifelong latent infection in sensor

10 nae subfamily members, bovine herpesvirus 1 (BHV-1) establishes latency in sensory neurons.

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

14 Bovine herpesvirus 1 (BHV-1) induces immune suppression, but the mechanisms fo

15 Bovine herpesvirus 1 (BHV-1) induces PCD in peripheral blood mononuclear cells

16 Bovine herpesvirus 1 (BHV-1) infected cell protein 0 (bICP0) stimulates produc

17 g acute infection, the bovine herpesvirus 1 (BHV-1) infection cycle is blocked in sensory ganglionic

18 Bovine herpesvirus 1 (BHV-1) infection induces clinical symptoms in the upper

19 Bovine herpesvirus 1 (BHV-1) infection induces clinical symptoms in the upper

20 Bovine herpesvirus 1 (BHV-1) is an important pathogen of cattle and infection

21 Bovine herpesvirus 1 (BHV-1) is an important pathogen of cattle, and infection

22 Bovine herpesvirus 1 (BHV-1) is an important pathogen of cattle, and infection

23 ed transcript (LRT) of bovine herpesvirus 1 (BHV-1) is the only abundant viral RNA detected during la

24 e the primary site for bovine herpesvirus 1 (BHV-1) latency.

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

28 The bovine herpesvirus 1 (BHV-1) U(L)3.5 gene encodes a 126-amino-acid tegument pr

29 The bovine herpesvirus 1 (BHV-1) UL49 gene encodes a viral tegument protein termed

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

32 Bovine herpesvirus 1 (BHV-1), an alphaherpesvirinae subfamily member, establis

33 Bovine herpesvirus 1 (BHV-1), like other Alphaherpesvirinae subfamily members,

34 Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae sub

35 Bovine herpesvirus 1 (BHV-1), like other members of the Alphaherpesvirinae sub

36 abies virus (PRV), and bovine herpesvirus 1 (BHV-1).

37 ave been identified in bovine herpesvirus 1 (BHV-1).

38 rabies virus (PRV) and bovine herpesvirus 1 (BHV-1).

39 Bovine herpesvirus type 1 (BHV-1) is an important component of the bovine respirato

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

44 We used the bovine herpes virus 1 (BHV-1) latency-related (LR) gene, which was previously s

45 ng the model pathogen Bovine Herpes Virus-1 (BHV-1) this study employs an extended-gate field-effect

46 alpha-transinducing factor (alphaBTIF) as a BHV-1 U(L)3.5-interacting protein.

47 We have constructed a BHV-1 bacterial artificial chromosome (BAC) clone by ins

48 surface to serve as a capture antigen for a BHV-1-specific antibody (anti-gE), produced in cattle in

49 Consequently, we hypothesized that a BHV-1 infection might induce events in neurons which occ

50 This strongly suggests that a BHV-1 LR gene function was able to efficiently substitut

51 pecifically with antibodies prepared against BHV-1 U(L)49.5, previously reported to be a 9-kDa protei

52 Like other alphaherpesviruses, BHV-1 establishes latency in sensory neurons but has the

53 Consequently, we analyzed BHV-1 gene expression in bovine TG at 1, 2, 4, 7, and 15

54 l help define VP22 function within HSV-1 and BHV-1 infection.

55 EHV-1 and BHV-1 Us9 were able to fully compensate for the loss of

56 ), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressing BHV-5 gE (BHV-1gE5).

57 eptor (Pvr) itself mediated entry of PRV and BHV-1 but not of the HSV strains tested.

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,

60 gDs but did not impair the entry of PRV and BHV-1.

61 ti-gE present in commercially available anti-BHV-1 antiserum and in real serum samples from cattle wi

62 When both BHV-1.1 proteins were expressed in a coinfection, all re

63 t in viral egress but can be complemented by BHV-1 U(L)3.5.

64 but not CD8(+) lymphocytes were infected by BHV-1 as judged by in situ hybridization and PCR, respec

65 within the CNS and could not be replaced by BHV-1 gE.

66 esis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gED

67 Despite these differences, BHV-1 Us9 not only complemented for BHV-5 Us9 and rescue

68 t VP22 may have a modulatory function during BHV-1 infection.

69 Each BHV-1 gene was cloned in a PRV mutant lacking both the P

70 We sought to express BHV-1 open reading frame U(L)10, which encodes gM, and s

71 leted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressing BHV-5 gE (BHV-

72 Rabbits infected with BHV-5 expressing BHV-1 Us9 showed severe neurological signs at 5 days pos

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

75 lowing acute infection, the primary site for BHV-1 latency is the sensory neuron.

76 As judged by in situ hybridization, BHV-1-positive neurons were detected in trigeminal gangl

77 on mass spectrometry analysis, we identified BHV-1 alpha-transinducing factor (alphaBTIF) as a BHV-1

78 The function of BHV-1 U(L)3.5 in BHV-1 replication is not known.

79 virus from the nose or eyes and increases in BHV-1-specific antibodies.

80 uggests that VP22 plays a functional role in BHV-1 replication.

81 fraction of pulse-labeled gI synthesized in BHV-1-infected cells apparently is cleaved into two rela

82 three proteins being longer in BHV-5 than in BHV-1.

83 Finally, we incubated BHV-1-infected cell extracts with nonimmune mouse, rabbi

84 Following acute infection, BHV-1 establishes latency in sensory neurons within trig

85 Following acute infection, BHV-1 establishes latency in sensory neurons within trig

86 MC) of cattle immunized with attenuated live BHV-1.

87 In this study, we show that mature BHV-1 Us9 is a 30- to 32-kDa protein, whereas mature BHV

88 d compared with that of the nonneurovirulent BHV-1.

89 The ability of BHV-1 to transport anterogradely from neuronal cell bodi

90 We examined the induction and activity of BHV-1-specific cytolytic CD4(+) T lymphocytes (CTL) by s

91 Apoptosis of BHV-1-expressing target cells was observed in CD4(+) CTL

92 part, because it activates all 3 classes of BHV-1 genes.

93 nt role in the latency reactivation cycle of BHV-1 in cattle.

94 Second, expression of BHV-1.1 gE alone facilitated PRV infection of a subset o

95 The function of BHV-1 U(L)3.5 in BHV-1 replication is not known.

96 the pathogenesis of BRDC and maintenance of BHV-1 in the cattle population.

97 gE in the differential neuropathogenesis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 rec

98 ant of the differential neuropathogenesis of BHV-1 and BHV-5.

99 mportant role in the latency/pathogenesis of BHV-1, construction of a mutant is necessary to test thi

100 First, the presence of BHV-1.1 gI alone, but not PRV gI alone, promoted viral i

101 dramatic effects on the growth properties of BHV-1.

102 ifferent from the corresponding gE region of BHV-1.

103 ent of the predicted amino acid sequences of BHV-1 and BHV-5 gE open reading frames showed that they

104 ared with the corresponding Us9 sequences of BHV-1.1.

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.

109 HSV-2 entry but not for the entry of PRV or BHV-1.

110 that observed after infection with parental BHV-1, and there were no observable differences in proce

111 ollowing dexamethasone-induced reactivation, BHV-1 induces expression of cyclin A in neurons.

112 A BAC-excised, reconstituted BHV-1 containing only the 34-bp loxP sequence within the

113 lasmic tail-truncated BHV-1 and a gE-rescued BHV-1.

114 Since BHV-1 can induce apoptosis of cultured lymphocytes, we h

115 Taken together, these results indicate that BHV-1 can infect CD4(+) T cells in cattle, leading to ap

116 The BHV-1 LR gene inhibited cell cycle progression and proli

117 The BHV-1, EHV-1, and PRV proteins complement ICP0-null muta

118 rom the HSV-1 VP16 response element, and the BHV-1 VP16 protein activates transcription from the BHV-

119 All recombinant viruses expressed the BHV-1 proteins at levels similar to or greater than that

120 t CD2(+) T lymphocytes were positive for the BHV-1 envelope glycoprotein gD.

121 P16 protein activates transcription from the BHV-1 VP16 response element.

122 Interestingly, the BHV-1 VP22 deletion mutant virus is asymptomatic and avi

123 d CJLAT, contains two complete copies of the BHV-1 LR gene (one in each viral long repeat) in place o

124 Attenuation of the BHV-1 VP22 deletion mutant virus in vivo suggests that V

125 We examined the ability of the BHV-1.1 gE and gI homologs to direct circuit-specific in

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

128 This suggested that the BHV-1 LR gene and the HSV-1 LAT gene are not functionall

129 We have shown previously that the BHV-1.1 gE and gI proteins are capable of complementing

130 identify the proteins that interact with the BHV-1 U(L)3.5 protein.

131 BHV-5 is very similar to BHV-1, the etiological agent of infectious bovine rhinot

132 The highest similarity to BHV-1 products (>or=95% amino acid identity) is found in

133 he sensor capabilities as a diagnostic tool, BHV-1 viral protein gE was expressed and immobilized on

134 constructed a gE cytoplasmic tail-truncated BHV-1 and a gE-rescued BHV-1.

135 t seizure model that distinguished wild-type BHV-1 and -5 based on their differential neuropathogenes

136 In contrast to BHV-5, wild-type BHV-1 failed to invade the CNS following intranasal infe

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

139 In vitro, BHV-1 Us9 is expressed at 3 h postinfection (hpi), where

140 To test whether BHV-1 persisted in lymphoreticular tissue, we analyzed t

141 The mechanism by which BHV-1 induces PCD in peripheral blood mononuclear cells

142 infection of bovine kidney (MDBK) cells with BHV-1 leads to PCD, as judged by terminal deoxynucleotid

143 Calves infected with BHV-1 for 7 days revealed increased apoptotic cells near

144 ut not allogeneic, macrophages infected with BHV-1 or pulsed with BHV-1 polypeptides.

145 anglia (TG) of calves latently infected with BHV-1 versus DEX-treated animals.

146 cells (PBMC) after calves were infected with BHV-1.

147 e treatment of calves latently infected with BHV-1.

148 that CD4(+) CTL lyse macrophages pulsed with BHV-1 polypeptides through a Fas-mediated lytic pathway

149 crophages infected with BHV-1 or pulsed with BHV-1 polypeptides.

150 xpressed bICP0 at least as efficiently as WT BHV-1 or the LR rescued virus.

151 Relative to wt BHV-1, the LR mutant did not induce explant-induced reac

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

155 esults to those from calves infected with wt BHV-1 or the LR-rescued virus.

156 is in TG compared to calves infected with wt BHV-1 or to mock-infected calves.

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