ライフサイエンスコーパス: IBV

1 IBV 3a protein is expressed in infected cells but is not

2 IBV infection induced antibodies specific to the HA head

3 IBV is an important human pathogen, but its ability to i

4 IBV was derived by use of coronary resistance measuremen

5 IBV was detected in 3 nasal swabs from PRRSV-seropositiv

6 IBV-specific CTL epitopes were mapped within the carboxy

7 In addition, IBV was detected in 3 nasal swabs collected from PRRSV-s

8 vaccine provides complete protection against IBV strains.

9 Although IBV has been isolated from seals, humans are considered

10 single tube/well (IBV genomic amplification [IBV-GA]).

11 Using an IBV reverse genetics system, we demonstrated that the te

12 observations made with other coronavirus and IBV N proteins with both overexpressed proteins and infe

13 omparison of crystal packing of SARS-CoV and IBV N-NTDs suggests a common mode of RNA recognition, bu

14 The availability of attenuated IAV and IBV backbones based on contemporary strains offers alter

15 segmented negative-sense RNA genome from any IBV strain in a single tube/well (IBV genomic amplificat

16 d a panel of pathogenic, mild and attenuated IBV strains in ex vivo tracheal organ culture (TOC).

17 n patients selected because of high baseline IBV.

18 P < 0.001) and patients with large baseline IBV showed substantial and clinically significant reduct

19 in IBV was directly related to the baseline IBV (r2 = 0.97; P < 0.001) and patients with large basel

20 ally, disruption of the secretory pathway by IBV E correlates with a form that is likely monomeric, s

21 in in vitro, indicating that host shutoff by IBV plays an important role in antagonizing the host's i

22 of amplifying the diverse and ever-changing IBV genome, we developed and optimized techniques that a

23 ics, antiviral drugs, and vaccines to combat IBV.

24 navirus and demonstrate that the coronavirus IBV employs a direct, low-pH-dependent virus-cell fusion

25 lippery sequence variants of the coronavirus IBV frameshift signal in strains of Escherichia coli una

26 between coronary resistance- and MCE-derived IBV could yield insight into structural mechanisms of IB

27 Two antigenically distinct IBV hemagglutinin (HA) lineages cocirculate worldwide wi

28 Amplicons for >1,000 diverse IBV genomes from different sample types (e.g., clinical

29 olgi complex in cells transiently expressing IBV E.

30 genus and proposes the existence of a fifth IBV accessory protein.

31 tested swine serum samples were positive for IBV antibodies.

32 f a fifth, novel, group-specific protein for IBV.

33 ays of R18-labeled virions and show that for IBV, coronavirus-cell fusion occurs in a low-pH-dependen

34 stem 1 and to convert a short non-functional IBV-derived pseudoknot into a highly efficient, kinked f

35 study demonstrates that the gammacoronavirus IBV, similar to its mammalian counterparts, has evolved

36 dy closes a gap in the understanding of host-IBV interaction and paves the way for further characteri

37 ation of swine as a potential host for human IBV.

38 oexpressed with IBV M, both from cDNA and in IBV infection, the two proteins are colocalized in Golgi

39 To determine whether changes in IBV could be quantified in vivo, the left anterior desce

40 hocardiography (MCE) can quantify changes in IBV during coronary stenosis and (2) the relation betwee

41 MCE can quantify autoregulatory increases in IBV that maintain resting myocardial perfusion.

42 through both MDA5 and TLR3 remains intact in IBV-infected cells.

43 the ERGIC, similar to the dilysine motif in IBV S.

44 er, the localization of selected proteins in IBV-infected cells as well as their activity during viru

45 However, the reduction in IBV was directly related to the baseline IBV (r2 = 0.97;

46 of modulating stem 1 length and stability in IBV-based pseudoknots, and found that a stem 1 with at l

47 The Indian IBV isolate exhibited a relatively high degree of sequen

48 her closely related avian coronaviruses like IBV cause respiratory disease.

49 emonstrate that, in a time-dependent manner, IBV effectively interferes with IFN signaling and that i

50 MCE-IBV was calculated from microbubble transit rates.

51 trols, patients with TBI had a higher median IBV (56 [range, 9-281] vs 1 [range, 0-11] mL; P < .001)

52 vidence that accessory proteins 3a and 3b of IBV modulate the response at the transcriptional and tra

53 we demonstrate that accessory protein 5b of IBV plays a crucial role in the onset of host shutoff.

54 tance of cellular proteins in the biology of IBV.

55 Further characterization of IBV-EG3 revealed that damaged particles appeared to accu

56 We generated a cDNA clone of IBV E and antibodies to the E protein to study its cell

57 Here, an infectious cDNA clone of IBV was used to address the importance of the S protein

58 Finally, we determined that the delivery of IBV S to the plasma membrane was reduced in cells infect

59 rnative LAIV platform for the development of IBV vaccines.IMPORTANCE A number of issues with regard t

60 P), shifted the steady-state distribution of IBV M from the Golgi complex to the ER.

61 lts indicated that the hydrophobic domain of IBV E alters the host secretory pathway to the apparent

62 brane domain nor the short lumenal domain of IBV E is required for Golgi targeting.

63 EG3 suggested that the hydrophobic domain of IBV E may be important for the forward trafficking of ca

64 er strains, suggesting that the evolution of IBV strains in general has been a complex, and as yet, p

65 vidence for two distinct oligomeric forms of IBV E, one essential for assembly and the other with a r

66 Two distinct lineages of IBV are distinguished, based on variation in hemagglutin

67 Moreover, both lineages of IBV were able to infect pigs under experimental conditio

68 d synthesis had no effect on localization of IBV M or other Golgi markers.

69 lipid synthesis overlaps the localization of IBV M, we asked whether perturbation of sphingolipids af

70 on of sphingolipids affected localization of IBV M.

71 ation and recruitment are dual mechanisms of IBV change.

72 yield insight into structural mechanisms of IBV change.

73 A high-order oligomer of IBV E is required for the production of virus-like parti

74 channel activity and the oligomerization of IBV E.

75 thermore, we observed that overexpression of IBV E, but not EG3, induced the disassembly of the Golgi

76 f the IFN response during the early phase of IBV infection, the signaling of nonself dsRNA through bo

77 The phenotype of IBV-EG3 suggested that the hydrophobic domain of IBV E m

78 ormation of two distinct oligomeric pools of IBV E in transfected and infected cells and the residues

79 virus (PRRSV) showed a higher prevalence of IBV antibodies in our 2014 survey.

80 ealed that, in contrast to the S1 protein of IBV, S1 proteins of enteric gammacoronaviruses recognize

81 nimal species can support the replication of IBV and serve as a reservoir.

82 present work, we describe the resistance of IBV to IFN and the potential role of accessory proteins

83 rameshift efficiency in vitro of a series of IBV-based pseudoknots whose stem 1 length was varied fro

84 sults suggest that the endocytosis signal of IBV S is essential for productive virus infection.

85 ating antibodies directed to the HA stalk of IBV contribute to cross-protective immunity to IBV of bo

86 om chickens infected with the Gray strain of IBV or inoculated with a DNA plasmid encoding nucleocaps

87 cells infected with the homologous strain of IBV.

88 ected with serologically distinct strains of IBV was dose responsive in a manner similar to that for

89 The short luminal N terminus of IBV E contains a consensus site for N-linked glycosylati

90 c antibodies revealed that the C terminus of IBV E is cytoplasmic and the N terminus is translocated.

91 otein, we developed a recombinant version of IBV in which the E protein was replaced by a mutant cont

92 inal sequences engineered into the optimized IBV-GA2 products also enable ligation-free cloning to ra

93 IBV were linearly related, MCE overestimated IBV derived from the vasodilatation model and underestim

94 Here, we show that, in humans, primary IBV infection with either lineage induces HA-specific an

95 hat independently of its accessory proteins, IBV inhibits IFN-mediated phosphorylation and translocat

96 in resistance to IFN, as its absence renders IBV less resistant to IFN treatment.

97 At constant flow, MCE and resistance IBV increased with stenosis.

98 Although MCE and resistance IBV were linearly related, MCE overestimated IBV derived

99 nd closes a gap in the understanding of some IBV virulence strategies.

100 conserved in TOCs, each of the other tested IBV strains produced DMVs, zippered ER and spherules.

101 stinfection and produced larger plaques than IBV.

102 Our results demonstrate that IBV has evolved multiple strategies to avoid the activat

103 mmunoprecipitation studies demonstrated that IBV 3a localized to the cytoplasm in a diffuse pattern a

104 Confocal microscopy demonstrated that IBV 3a puncta lined up along smooth endoplasmic reticulu

105 Surprisingly, we found that IBV E, but not EG3, dramatically reduced the delivery of

106 sceptible to IBV infections, indicating that IBV is a swine pathogen, and swine may serve as a natura

107 Sequence analysis predicted that IBV 3a was a membrane protein; however, only a fraction

108 We propose that IBV M is at least in part localized by retrieval mechani

109 Previously, we reported that IBV induces a delayed activation of the IFN response.

110 We show that IBV E is an integral membrane protein when expressed in

111 We show that IBV inhibits synthesis of host proteins, including that

112 We show that IBV is fairly resistant to the antiviral state induced b

113 In summary, we show that IBV uses multiple strategies to counteract the IFN respo

114 We further show that IBV was not inactivated, and fusion was unaffected, by p

115 Our results suggest that IBV 3a is partially targeted to a novel domain of the sm

116 This suggests that IBV E is associated with the Golgi matrix through intera

117 The IBV E protein is palmitoylated on one or two cysteine re

118 The IBV M protein is incorporated into these particles when

119 The IBV-induced host shutoff, however, does not require degr

120 hough E. coli ribosomes changed frame at the IBV signal (UUUAAAG) with an efficiency similar to that

121 ase is not required for frameshifting at the IBV signal and some other explanation is required to acc

122 of PB1, which is sufficient to attenuate the IBV.

123 ) and improved flow metabolism coupling, the IBV was small and clinically insignificant in the majori

124 e core, is oriented similarly to that in the IBV N-NTD, and is involved in crystal packing in the mon

125 explored whether analogous mutations in the IBV polymerase subunits would result in a stable virus w

126 Interestingly, the IBV S protein also contains a tyrosine-based endocytosis

127 reported that the hydrophobic domain of the IBV E protein, a putative viroporin, causes disruption o

128 The NTD of the IBV Gray strain at 1.3-A resolution exhibits a U-shaped

129 nstituent hairpins, and three mutants of the IBV pseudoknot.

130 terminal truncations, we determined that the IBV E Golgi targeting information is present between tai

131 Our results show that the IBV pseudoknot requires a higher force than its correspo

132 reases the kinetic barriers to unfolding the IBV pseudoknot, but has only a minor effect on the hairp

133 ressed using recombinant vaccinia virus, the IBV E protein is released from cells at low levels in se

134 When compared with tissue within the IBV compartment, the HBV compartment showed similar medi

135 Thus, even though IBV E is present at low levels in virions, it is apparen

136 V contribute to cross-protective immunity to IBV of both lineages.

137 To determine the susceptibility of pigs to IBV infection, we conducted a serological survey for U.S

138 ata demonstrate that pigs are susceptible to IBV infection; therefore, they warrant further surveilla

139 lts demonstrate that pigs are susceptible to IBV infections, indicating that IBV is a swine pathogen,

140 ual to or greater than that of the wild-type IBV pseudoknot.

141 was reduced in cells infected with wild-type-IBV compared to those infected with IBV-EG3.

142 the vasodilatation model and underestimated IBV calculated from the recruitment model.

143 fluenza A virus (IAV) and influenza B virus (IBV) cause substantial morbidity and mortality during an

144 Influenza B virus (IBV) causes annual influenza epidemics around the world.

145 Influenza B virus (IBV) causes seasonal epidemics in humans.

146 Although human influenza B virus (IBV) is a significant human pathogen, its great genetic

147 Influenza B virus (IBV) is considered a major human pathogen, responsible f

148 ruses including infectious bronchitis virus (IBV) contain a putative open reading frame (ORF), locali

149 p 3 coronavirus infectious bronchitis virus (IBV) contains a canonical dilysine endoplasmic reticulum

150 the coronavirus infectious bronchitis virus (IBV) contains a classic hairpin-type RNA pseudoknot that

151 ian coronavirus infectious bronchitis virus (IBV) contains two cis-acting signals essential for effic

152 ammacoronavirus infectious bronchitis virus (IBV) does induce host shutoff, and we find that its acce

153 function of the infectious bronchitis virus (IBV) E protein, we developed a recombinant version of IB

154 from the avian infectious bronchitis virus (IBV) has dramatic effects on the secretory system which

155 ammacoronavirus infectious bronchitis virus (IBV) has evolved under evolutionary pressure to evade an

156 the coronavirus infectious bronchitis virus (IBV) is localized to the Golgi complex when expressed ex

157 y, we show that infectious bronchitis virus (IBV) is resistant to IFN treatment and identify a role f

158 doknot found in infectious bronchitis virus (IBV) is typical of those that possess a long stem 1 of 1

159 ar targeting of infectious bronchitis virus (IBV) membrane proteins.

160 eractome of the infectious bronchitis virus (IBV) N protein was mapped using stable isotope labeling

161 Infectious bronchitis virus (IBV) ORF 3a is one such gene.

162 f a novel avian infectious bronchitis virus (IBV) strain, CU-T2.

163 omologous avian infectious bronchitis virus (IBV) structure.

164 L) responses to infectious bronchitis virus (IBV) were determined at regular intervals between 3 and

165 nucleocapsid of infectious bronchitis virus (IBV) were identified by using target cells infected with

166 athogenic avian infectious bronchitis virus (IBV) with a novel genotype in India.

167 N protein from infectious bronchitis virus (IBV), a prototype coronavirus.

168 While infectious bronchitis virus (IBV), a respiratory pathogen of chickens, is rather well

169 an coronavirus, infectious bronchitis virus (IBV), contains information for localization to the cis-G

170 mmacoronavirus, infectious bronchitis virus (IBV), induces a delayed activation of the IFN response i

171 ammacoronavirus infectious bronchitis virus (IBV), induces regions of ER that are zippered together a

172 cluding chicken infectious bronchitis virus (IBV), require specific alpha2,3-linked sialylated glycan

173 pseudoknot from infectious bronchitis virus (IBV), three constituent hairpins, and three mutants of t

174 rotein of avian infectious bronchitis virus (IBV), which contains a cis-Golgi targeting signal.

175 ian coronavirus infectious bronchitis virus (IBV).

176 he S protein of infectious bronchitis virus (IBV).

177 oultry pathogen infectious bronchitis virus (IBV).

178 The mutant virus, IBV-EG3, was defective in release of infectious virus pa

179 Changes in intramyocardial blood volume (IBV) mediate autoregulatory adaptations to coronary sten

180 pact bone volume and trabecular bone volume (IBV) in CT slices.

181 nificant fall in the ischaemic brain volume (IBV) (from 15 +/- 16 to 5 +/- 4 ml; P < 0.01) and improv

182 Estimated ischemic brain volume (IBV) and hypoxic brain volume (HBV) and a comparison of

183 e from any IBV strain in a single tube/well (IBV genomic amplification [IBV-GA]).

184 afficking of cargo, so we determined whether IBV E facilitated the delivery of cargo to the plasma me

185 When coexpressed with IBV M, both from cDNA and in IBV infection, the two prot

186 ild-type-IBV compared to those infected with IBV-EG3.

187 sociation of selected cellular proteins with IBV N protein was confirmed by immunoblotting, cosedimen

188 iciently and displayed cross-reactivity with IBV of both lineages.

189 Within IBV, coregistered PET data were extracted to identify th