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 vaccines are currently developed by serial passage o

5 IBV was derived by use of coronary resistance measuremen

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

7 IBV-specific CTL epitopes were mapped within the carboxy

8 gmRNA IR), which are widely conserved across IBV isolates.

9 s did not activate H3, but they did activate IBV HA in vitro Our results indicate that TMPRSS4 is an

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

11 nd spread of IBV in AECII but did not affect IBV activation in HBEC and Calu-3 cells.

12 ilarly broadly protective antibodies against IBV NA have not been identified.

13 ls have lower clinical effectiveness against IBV compared to influenza A viruses (IAV).

14 vaccine provides complete protection against IBV strains.

15 sal vaccine to replace live vaccines against IBV and other emerging coronaviruses.

16 While all IBV strains infect the chicken respiratory tract via the

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

18 te, engaging residues highly conserved among IBV NAs.

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

20 /2009 H1N1 and A/Wyoming/3/2003 H3N2) and an IBV (B/Brisbane/60/2008, Victoria lineage), demonstratin

21 antibodies (mAbs) that target IBV NA from an IBV-infected patient.

22 itro Our results indicate that TMPRSS4 is an IBV-activating protease in murine AECIIs and suggest tha

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

24 ng protease of IAV in human airway cells and IBV in type II pneumocytes and as a potential target for

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

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

27 , sets of murine proteases facilitate H3 and IBV HA cleavages.

28 MPRSS13, hepsin, and prostasin cleave H3 and IBV HA in mice.

29 SS13, hepsin, and prostasin activated H3 and IBV HA in vitro IBV activation and replication was reduc

30 of individual components of TIV- H1, H3, and IBV- with good correlation with the SRID method.

31 A(H1N1)pdm09 and IBV (6 cases), A(H3N2) and IBV (8 cases), and nonsubtyped IAV and IBV (3 cases); an

32 ) and IBV (8 cases), and nonsubtyped IAV and IBV (3 cases); and 1 case of triple infection with A(H3N

33 nd H1N1pdm IAV in mice but that H3N2 IAV and IBV activation is independent of TMPRSS2 and carried out

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

35 ate globally and infect humans, with IAV and IBV causing the most severe disease.

36 Multicycle replication of H3N2 IAV and IBV in AECIIs of Tmprss2/Tmprss4-deficient mice varied i

37 ry human bronchial cells and of both IAV and IBV in primary human type II pneumocytes.

38 TMPRSS2 in proteolytic activation of IAV and IBV in three human airway cell culture systems: primary

39 In contrast, activation of H3N2 IAV and IBV was found to be independent of TMPRSS2 expression an

40 et RPA system was designed to detect IAV and IBV, and its detection performance was fine-tuned.

41 Here, to identify additional H3 IAV- and IBV-activating proteases, we used RNA-Seq to investigate

42 amely TGN and ERGIC/cis-Golgi for MERS-M and IBV-M, respectively.

43 nza A(H3N2) virus (1 case), A(H1N1)pdm09 and IBV (6 cases), A(H3N2) and IBV (8 cases), and nonsubtype

44 le infection with A(H3N2), A(H1N1)pdm09, and IBV.

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

46 o develop mechanisms to rationally attenuate IBV for the next generation of effective vaccines.IMPORT

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

48 Influenza A (IAV) and influenza B (IBV) viruses are highly contagious pathogens that cause

49 evelop effective cross-reactive T-cell based IBV vaccines.

50 n patients selected because of high baseline IBV.

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

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

53 yltransferase 1 (B3GAT1), effectively blocks IBV infection.

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

55 Disruption of the secretory pathway by IBV E correlates with a form that is likely monomeric, s

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

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

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

59 A broader array of conserved IBV T-cell epitopes is needed to develop effective cross

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

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

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

63 To determine if any cells can survive direct IBV infection, we here generate a recombinant IBV capabl

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

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

66 can also replicate in the kidneys, dividing IBV into the following two pathotypes: nonnephropathogen

67 wo pathotypes: nonnephropathogenic (example, IBV-M41) and nephropathogenic viruses (including IBV-QX)

68 olgi complex in cells transiently expressing IBV E.

69 apsulation of plasmid DNA vaccine expressing IBV nucleocapsid (N) protein by the QAC adjuvant system

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

71 tested swine serum samples were positive for IBV antibodies.

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

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

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

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

76 The heavily glycosylated IBV spike protein is responsible for binding to host tis

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

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

79 f CD8(+) T cell cross-reactivity across IAV, IBV and ICV.

80 Influenza A, B and C viruses (IAV, IBV and ICV, respectively) circulate globally and infect

81 HA of most influenza A and B (IAV/IBV) viruses is cleaved at a monobasic motif by trypsin-

82 binding of QX-RBD to a previously identified IBV-M41 receptor was confirmed by enzyme-linked immunoso

83 st cell response to IBV infection.IMPORTANCE IBV is a major avian pathogen and presents a substantial

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

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

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

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

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

89 ndicating that murine TMPRSS4 is involved in IBV activation.

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

91 to kidney, while the reciprocal mutations in IBV-QX abolished kidney binding completely.

92 NA ORF1a/ORF1b junction revealed that PRF in IBV is highly efficient (33 to 40%).

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

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

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

96 M41) and nephropathogenic viruses (including IBV-QX).

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

98 splayed broad and potent capacity to inhibit IBV NA enzymatic activity, neutralize the virus in vitro

99 Intriguingly, IBV polymerase is able to use murine Anp32A.

100 e virus in vitro, and protect against lethal IBV infection in mice in prophylactic and therapeutic se

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

102 ently published cryo-EM structure of the M41 IBV spike protein and our glycosylation results revealed

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

104 MCE-IBV was calculated from microbubble transit rates.

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

106 ntly produced RBDs from the nephropathogenic IBV strain QX and from the nonnephropathogenic strain M4

107 ded for recombination and emergence of novel IBV serotypes.

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

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

110 lease of infectious virions, accumulation of IBV spike (S) protein on the plasma membrane compared to

111 tance of cellular proteins in the biology of IBV.

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

113 IBV-infected cells, and aberrant cleavage of IBV S on virions.

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

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

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

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

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

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

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

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

122 ine the within-host evolutionary dynamics of IBV by sequencing virus populations from naturally infec

123 is known about the evolutionary dynamics of IBV during individual infections and transmission events

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

125 Infection with IBV or expression of IBV E induces neutralization of Golgi pH, promoting a mo

126 idence suggesting that the monomeric form of IBV E correlates with an increased Golgi luminal pH.

127 with both pathogenic and attenuated forms of IBV and expand our understanding of gammacoronaviral gen

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

129 Mutation of the HD of IBV E in a recombinant virus background results in impai

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

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

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

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

134 on of sphingolipids affected localization of IBV M.

135 ation and recruitment are dual mechanisms of IBV change.

136 yield insight into structural mechanisms of IBV change.

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

138 channel activity and the oligomerization of IBV E.

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

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

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

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

143 ormation of two distinct oligomeric pools of IBV E in transfected and infected cells.

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

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

146 t with the lower global evolutionary rate of IBV.IMPORTANCE The evolution of influenza virus is a sig

147 tion of the receptor-binding domain (RBD) of IBV strain M41 spike protein and assessed the role of th

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

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

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

151 rves the epithelium to limit the severity of IBV disease.

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

153 also inhibited the activation and spread of IBV in AECII but did not affect IBV activation in HBEC a

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

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

156 M41-CK, a virulent lab-adapted strain of IBV, was egg passaged over 100 times in four parallel in

157 cells infected with the homologous strain of IBV.

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

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

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

161 for the extended nephropathogenic tropism of IBV-QX.

162 ill be aided by an improved understanding of IBV molecular biology.

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

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

165 el epitopes were readily detected in IAV- or IBV-infected pediatric and adult subjects.

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

167 f four replicates of a serially egg-passaged IBV revealed a different pattern of genomic variation in

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

169 teraction with host cell factors, protecting IBV S from premature cleavage and leading to the efficie

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

171 BV infection, we here generate a recombinant IBV capable of activating a host-cell reporter to perman

172 s 110 to 112 (KIP) were sufficient to render IBV-M41 with the ability to bind to kidney, while the re

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

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

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

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

177 While some IBV strains replicate locally, others can disseminate to

178 man monoclonal antibodies (mAbs) that target IBV NA from an IBV-infected patient.

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

180 stinfection and produced larger plaques than IBV.

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

182 Using this system, we demonstrate that IBV infection leads to the formation of a survivor cell

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

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

185 protein secretion profiles demonstrated that IBV-inoculated FNEC expressed delayed type-I/II IFN resp

186 1 individuals with influenza B, we find that IBV accumulates lower genetic diversity than previously

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

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

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

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

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

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

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

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

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

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

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

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

199 e-validated transmission pairs suggests that IBV experiences a tight transmission bottleneck similar

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

201 The IBV M protein is incorporated into these particles when

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

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

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

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

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

207 RiboSeq) to delineate gene expression in the IBV M41-CK and Beau-R strains at subcodon resolution.

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

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

210 howed that overall sequence diversity in the IBV population increased but the four replicates only ha

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

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

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

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

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

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

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

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

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

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

221 , however the responses of CD8(+) T cells to IBV and ICV are understudied.

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

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

224 vide insights into the host cell response to IBV infection.

225 ving insights into the host cell response to IBV infection.IMPORTANCE IBV is a major avian pathogen a

226 lls indicated that the host cell response to IBV occurs primarily at the level of transcription, with

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

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

229 the viral attachment protein spike from two IBV strains with different tropisms.

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

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

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

233 used in the rational attenuation of virulent IBV for next-generation vaccine design.

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

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

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

237 fluenza A virus (IAV) and influenza B virus (IBV) HA possessing a monobasic cleavage site.

238 Influenza B virus (IBV) infections can cause severe disease in children and

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

240 Influenza B virus (IBV) is an acute, respiratory RNA virus that has been as

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

242 fluenza A virus (IAV) and influenza B virus (IBV) replication in human cells.

243 Influenza B virus (IBV) undergoes seasonal antigenic drift more slowly than

244 s (IAV), group 2 IAV, and influenza B virus (IBV) were designed and produced in bacterial recombinant

245 nfluenza A virus (IAV) or influenza B virus (IBV).

246 ines to control infectious bronchitis virus (IBV) and other poultry pathogens.

247 ammacoronavirus infectious bronchitis virus (IBV) causes an acute, highly contagious respiratory dise

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

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

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

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

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

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

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

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

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

257 Infectious bronchitis virus (IBV) infects ciliated epithelial cells in the chicken re

258 (IB) caused by infectious bronchitis virus (IBV) is currently a major threat to chicken health, with

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

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

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

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

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

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

265 aviruses, avian infectious bronchitis virus (IBV) possesses a long, single-stranded, positive-sense R

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

267 omologous avian infectious bronchitis virus (IBV) structure.

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

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

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

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

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

273 uses, including infectious bronchitis virus (IBV), are important respiratory pathogens of poultry.

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

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

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

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

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

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

280 oultry pathogen infectious bronchitis virus (IBV).

281 ian coronavirus infectious bronchitis virus (IBV).

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

283 he M protein of infectious bronchitis virus (IBV).

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

285 nza A viruses (IAV) and influenza B viruses (IBV) cause significant morbidity and mortality during se

286 d prostasin activated H3 and IBV HA in vitro IBV activation and replication was reduced in AECIIs fro

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

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

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

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

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

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

293 tion of Golgi pH, promoting a model in which IBV E alters the secretory pathway through interaction w

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

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

296 Infection with IBV or expression of IBV E induces neutralization of Gol

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

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

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

300 e plasma membrane compared to wild-type (WT) IBV-infected cells, and aberrant cleavage of IBV S on vi