ライフサイエンスコーパス: influenza B virus

1 that possessed HA, NA, or both HA and NA of influenza B virus.

2 ss and recent resurgence of epidemics due to influenza B virus.

3 8% and 98.3% and 100% and 100% for detecting influenza B virus.

4 yielded influenza A virus, and 1.1% yielded influenza B virus.

5 n of influenza A virus and the HA protein of influenza B virus.

6 for influenza A/2009/H1N1 virus, and 95% for influenza B virus.

7 influenza A virus and 15 were infected with influenza B virus.

8 tality after challenge with a lethal dose of influenza B virus.

9 e for the inhibition of ISG15 conjugation by influenza B virus.

10 H1 and H3 strains of influenza A, as well as influenza B virus.

11 segments of two highly homologous strains of influenza B virus.

12 d of IFN-alpha/beta synthesis than wild-type influenza B virus.

13 ) viruses carrying the neuraminidase (NA) of influenza B virus.

14 se-negative results were found to be growing influenza B virus.

15 oproteins from either of the two lineages of influenza B virus.

16 pared with controls immunized with unrelated influenza B virus.

17 rom an immunocompromised child infected with influenza B virus.

18 virus strains as well as with the NS1 of an influenza B virus.

19 s hospitalised with influenza A H1N1pdm09 or influenza B virus.

20 ENIA) for rapid detection of influenza A and influenza B viruses.

21 culating, antigenically distinct lineages of influenza B viruses.

22 amino acids that are highly conserved among influenza B viruses.

23 nces after vaccination were observed against influenza B viruses.

24 nn Arbor/1/66 were aligned to those of other influenza B viruses.

25 iruses, and 53% (95% CI, 43% to 61%) against influenza B viruses.

26 commonly cross-reacted with H3N2 viruses and influenza B viruses.

27 inhibition assay and microneutralisation for influenza B viruses.

28 ilable for antibodies that broadly recognize influenza B viruses.

29 c influenza A viruses and stalk domains from influenza B viruses.

30 protected from lethal challenge with diverse influenza B viruses.

31 ls to determine the fitness of NAI-resistant influenza B viruses.

32 tive capacities and fitness of NAI-resistant influenza B viruses.

33 ection of influenza A virus (76.4%) than for influenza B virus (40.9%).

34 raminidase subtypes of influenza A virus and influenza B virus (41 influenza virus strains) and 24 co

35 Altogether, opposite-lineage influenza B viruses accounted for 10.8% of all influenza

36 iruses was associated with increased risk of influenza B virus acquisition.

37 nfection who were subsequently infected with influenza B virus after a mean interval of 50 days.

38 The segmented genome of influenza B virus allows exchange of gene segments betwe

39 ed 95% sensitivity for influenza A virus and influenza B virus and 95 and 97% specificity compared to

40 98%, respectively, but the sensitivities for influenza B virus and adenovirus were unacceptable (14.3

41 describe a novel Asp198Asn NA mutation in an influenza B virus and its decreased susceptibility to bo

42 more vulnerable to heterologous infections (influenza B virus and MRSA) than those born to PBS- or p

43 s, human coronavirus, human metapneumovirus, influenza B virus and respiratory syncytial virus.

44 ibute to fatal outcomes after infection with influenza B virus and that the frequency of these manife

45 idual donors were successfully infected with influenza B virus and then inoculated with serogroup B N

46 ility to viral infection, and in the case of influenza B virus and vaccinia virus, ISG15 conjugation

47 reliable genome mapping of highly homologous influenza B viruses and (ii) extensive monitoring of inf

48 for isolation and productive replication of influenza B viruses and determine the biological and gen

49 eassortment plays a role in the evolution of influenza B viruses and may necessitate a change in the

50 0% for influenza A virus, 100% and 99.7% for influenza B virus, and 100% and 100% for respiratory syn

51 were 98.1% for influenza A virus, 98.0% for influenza B virus, and 97.7% for RSV.

52 esses determine the evolutionary dynamics of influenza B virus, and how influenza viruses A and B int

53 ssential for signaling by influenza A virus, influenza B virus, and human respiratory syncytial virus

54 nn Arbor, MI), that typed influenza A virus, influenza B virus, and respiratory syncytial virus (RSV)

55 Northbrook, IL) to detect influenza A virus, influenza B virus, and respiratory syncytial virus A and

56 c, and rapid detection of influenza A virus, influenza B virus, and RSV and subtyping of influenza A

57 ive percent agreement for influenza A virus, influenza B virus, and RSV were 79.2% (95% confidence in

58 t the splicing biology of influenza A virus, influenza B virus, and Salmon isavirus, revealing a comm

59 ng influenza A viruses H1N1, H3N2, and H5N1, influenza B viruses, and other respiratory viruses.

60 nd mechanism of action of broadly protective influenza B virus antibodies is required to inform vacci

61 lly distinct 'Yam88' and 'Vic87' lineages of influenza B virus are the result of changes in herd immu

62 Influenza B viruses are important human pathogens that r

63 Influenza B viruses are important human respiratory path

64 ) was found to phylogenetically cluster with influenza B viruses as a sister clade.

65 cytotoxicity and in vivo protection against influenza B viruses belonging to both haemagglutinin lin

66 Influenza A virus M2 (A/M2) and the influenza B virus BM2 are both small integral membrane p

67 The influenza B virus BM2 proton-selective ion channel is es

68 However, NP of influenza B viruses (BNP) contains an evolutionarily con

69 Furthermore, potent inhibition of influenza B viruses but not other RNA or DNA viruses was

70 and amphibians cluster as a sister clade of influenza B viruses but remain largely uncharacterized.

71 trains, several swine influenza viruses, and influenza B viruses but were not overtly susceptible to

72 n and its disease severity is worse than the influenza B virus, but similar to influenza A virus asso

73 Only one specimen was determined to contain influenza B virus by Hexaplex; it was tissue culture neg

74 arliest step in innate immune recognition of influenza B virus by human macrophages.

75 Unlike most virulent wild-type (wt) influenza B viruses, ca B/Ann Arbor/1/66 is temperature

76 full-length hemagglutinin (HA) of prototype influenza B viruses can complement the function of multi

77 Here we demonstrate that influenza B viruses can replicate in the upper respirato

78 o single-cycle infectious influenza A virus, influenza B virus cannot incorporate heterotypic transge

79 Human infections with influenza B viruses carrying the E119A or H274Y substitu

80 Influenza B viruses cause seasonal epidemics and are a c

81 Influenza B virus causes a significant amount of morbidi

82 Influenza B virus causes annual epidemics and, along wit

83 Together with the influenza A virus, influenza B virus causes seasonal flu epidemics.

84 Influenza B virus causes significant disease but remains

85 and C9, to identify the cellular tropism of influenza B virus, characterize concomitant bacterial pn

86 fluenza A(H1N1)pdm09, influenza A(H3N2), and influenza B viruses circulating in 2009 and 2010.

87 We sequenced 72 influenza B viruses collected in Kuala Lumpur, Malaysia,

88 or influenza A viruses and 81.80% (9/11) for influenza B viruses compared to those for an in-house re

89 the influenza A, influenza A 2009 H1N1, and influenza B viruses compared to those of culture were 90

90 N2 (phylogenetic group 2 hemagglutinin), and influenza B virus components.

91 e NP of influenza A and B viruses, the NP of influenza B virus contains an evolutionarily conserved 5

92 These results support the notion that influenza B viruses continued to evolve through antigeni

93 es with a high load of nontarget template or influenza B virus, demonstrating assay specificity.

94 amework has until now not been available for influenza B viruses, despite their significant disease b

95 In conclusion, influenza B virus did not increase association of serogr

96 with either an H1N1 influenza A virus or an influenza B virus did so.

97 Influenza B virus encodes non-structural protein 1 (NS1B

98 Segment 7 of influenza B virus encodes two proteins, M1 and BM2.

99 e mechanisms are activated immediately after influenza B virus entry through the endocytic pathway, w

100 Influenza B virus evolves more slowly than influenza A v

101 Of note, we rescued recombinant influenza B viruses expressing mosaic B hemagglutinins,

102 a indicate that the chimeric live-attenuated influenza B viruses expressing the modified influenza A

103 tral in shaping the evolutionary dynamics of influenza B virus, facilitating the shift of dominance b

104 Influenza A and influenza B viruses (FLUAVs and FLUBVs, respectively) ut

105 Here, we report the construction of mutant influenza B viruses for potential use as improved live-v

106 The BM2 protein of influenza B virus functions as an ion channel, which is

107 ly lead to circulation of 3 or more distinct influenza B viruses, further complicating influenza vacc

108 e evidence suggesting a similar mechanism of influenza B virus genome packaging.

109 By analyzing over 12,000 influenza B virus genomes, we describe the processes ena

110 nza A virus packaging signals to full-length influenza B virus glycoproteins, we rescued influenza A

111 Furthermore, these structures of influenza B virus HA are compared with known structures

112 Here we report the structures of influenza B virus HA in complex with human and avian rec

113 The native influenza B virus HA segment could not be incorporated i

114 B virus HA molecules and for the ability of influenza B virus HA to distinguish human and avian rece

115 The structure of influenza B virus HA with avian receptor analog also rev

116 years, infected with A/H1N1pdm09, A/H3N2 or influenza B virus had prolonged viral RNA shedding (+/-1

117 Influenza B virus has been less studied than influenza A

118 e than two dozen amino acid substitutions on influenza B virus HAs have been identified to cause anti

119 The fitness of NAI-resistant influenza B viruses has not been widely studied.

120 nal antibodies against the haemagglutinin of influenza B viruses have been described, none targeting

121 Influenza B viruses have been documented to circulate on

122 Influenza B viruses have circulated in humans for over 8

123 Influenza B virus hemagglutinin (BHA) contains a predict

124 t further highlights that a broadly reactive influenza B virus hemagglutinin (HA) antigen stimulates

125 Here, we investigated four influenza B virus hemagglutinin (HA) head specific, hema

126 The influenza B virus hemagglutinin contains four major anti

127 genic sites and the noncanonical epitopes of influenza B virus hemagglutinin in animals and humans us

128 In order to identify residues on the influenza B virus hemagglutinin interacting with the MAb

129 eletions (indels), as observed frequently in influenza B virus hemagglutinin, had little effect on an

130 ive, nonneutralizing antibodies specific for influenza B virus hemagglutinin.

131 s that bind to the conserved stalk domain of influenza B virus hemagglutinin.

132 group 1 hemagglutinins but also group 2 and influenza B virus hemagglutinins.

133 ry viruses, in particular influenza A virus, influenza B virus, HMPV, and RSV.

134 n certain species may contribute to limiting influenza B virus host range.

135 Influenza A virus (IAV) and influenza B virus (IBV) cause substantial morbidity and

136 Influenza B virus (IBV) causes annual influenza epidemic

137 Influenza B virus (IBV) causes seasonal epidemics in hum

138 TMPRSS2 cleaves influenza A virus (IAV) and influenza B virus (IBV) HA possessing a monobasic cleava

139 Influenza B virus (IBV) infections can cause severe dise

140 Although human influenza B virus (IBV) is a significant human pathogen,

141 Influenza B virus (IBV) is an acute, respiratory RNA vir

142 Influenza B virus (IBV) is considered a major human path

143 ividuals born between 1917 and 2008, against influenza B virus (IBV) isolates from 1940 to 2021.

144 Here, we generated mRNA vaccine encoding influenza B virus (IBV) neuraminidase (NA) conjugated to

145 ammalian-adapted influenza A virus (IAV) and influenza B virus (IBV) replication in human cells.

146 Influenza B virus (IBV) undergoes seasonal antigenic dri

147 1 influenza A virus (IAV), group 2 IAV, and influenza B virus (IBV) were designed and produced in ba

148 e respiratory coronavirus 2 (SARS-CoV-2) and influenza B virus (IBV), we validate the structure and c

149 were positive for influenza A virus (IAV) or influenza B virus (IBV).

150 Most people are exposed to influenza A and influenza B viruses (IBV) at an early age through natura

151 Influenza B viruses (IBV) can cause severe disease and d

152 ons.IMPORTANCE Influenza A viruses (IAV) and influenza B viruses (IBV) cause significant morbidity an

153 Influenza B viruses (IBV) cocirculate with influenza A v

154 idly evolving influenza A viruses (IAVs) and influenza B viruses (IBVs) are major causes of recurrent

155 Influenza B viruses (IBVs) cause substantive morbidity a

156 Influenza B viruses (IBVs) comprise a substantial portio

157 s that could induce broad protection against influenza B viruses.IMPORTANCE While broadly protective

158 1 strain, the 2009 pandemic H1N1 strain, and influenza B virus in cytotoxicity assays and intracellul

159 Successful uncoating of the influenza B virus in endosomes is predicted to require a

160 the influenza A, influenza A 2009 H1N1, and influenza B viruses in approximately 70 min with minimal

161 easonal H1N1 (H1N1-s), influenza A H3N2, and influenza B viruses in nasopharyngeal swab (NPS) specime

162 Reassortment of influenza B viruses in nature as a means of genetic vari

163 after cell transfer with a noncross-reactive influenza B virus induced some of the donor D(b)NP(366)(

164 Influenza A virus, but not influenza B virus, induced increased production of IFN-b

165 Influenza B virus-induced activation of IRF3 required th

166 pattern recognition receptor needed for the influenza B virus-induced activation of IRF3.

167 We show that influenza B virus induces IFN regulatory factor 3 (IRF3)

168 We show that influenza B virus induces IRF3 activation, leading to IF

169 We show that influenza B virus induces the synthesis in human cells o

170 ic influenza A(H1N1) virus (A[H1N1]pdm09) or influenza B virus infection (P = .2 and .4, respectively

171 Here we analyzed the early events in influenza B virus infection and interferon (IFN) gene ex

172 Influenza B virus infection causes rates of hospitalizat

173 s could be a useful tool to treat or prevent influenza B virus infection in pediatric cohorts or in a

174 18 years; however, the pathogenesis of fatal influenza B virus infection is poorly described.

175 ablished immunocompromised murine models for influenza B virus infection that will facilitate evaluat

176 Finally, we demonstrate that ISG15 controls influenza B virus infection through its action within ra

177 at autopsy from 45 case patients with fatal influenza B virus infection were evaluated by light micr

178 virus infection was diagnosed in 3.5% (71), influenza B virus infection, in 0.9% (19); and influenza

179 /-) mice display increased susceptibility to influenza B virus infection, including non-mouse-adapted

180 talization due to influenza A(H1N1)pdm09 and influenza B virus infection, respectively.

181 loped an immunocompromised murine models for influenza B virus infection, which we subsequently used

182 of ISRE-controlled genes, is activated after influenza B virus infection.

183 a type, with demonstrated protection against influenza B virus infection.

184 vey, P = 0.01; immunology, P = 0.02) but not influenza B virus infection.

185 ion may not provide cross-protection against influenza B virus infection.

186 a viable strategy to broadly protect against influenza B virus infection.IMPORTANCE While current inf

187 g oseltamivir is less effective for treating influenza B virus infections than for treating influenza

188 viral resistance against vaccinia virus and influenza B virus infections.

189 .6% had influenza A H1N1pdm09, and 17.7% had influenza B virus infections; 16.7% required ICU admissi

190 Influenza B virus infects only humans and some marine ma

191 ARI in admitted patients were attributed to influenza B virus, influenza A virus, human metapneumovi

192 in antiviral response because a human virus, influenza B virus, inhibits ISG15 conjugation.

193 Influenza B virus is a human pathogen responsible for si

194 Influenza B virus is a serious health concern for childr

195 by RIG-I receptor, meaning that the incoming influenza B virus is already able to activate IFN gene e

196 The NB protein of influenza B virus is thought to function as an ion chann

197 The countermeasure by influenza B virus is unique in that it exhibits species

198 case for influenza A virus, transmission of influenza B viruses is enhanced at colder temperatures,

199 nd the neuraminidase of different strains of influenza B viruses is observed.

200 The evolution of influenza B viruses is poorly understood.

201 tween the vaccine and circulating strains of influenza B viruses is substantial, especially among chi

202 es broad and long-lasting protection against influenza B viruses is therefore urgently needed.

203 evolutionary analyses of all 11 genes of 31 influenza B viruses isolated from 1979 to 2003 were used

204 nin (HA) and neuraminidase (NA) sequences of influenza B viruses isolated in Guangzhou, a southern Ch

205 The majority of these antibodies recognized influenza B viruses isolated over the period of 73 years

206 In this study, influenza B viruses isolated within the past 10 years fr

207 Importantly, human H1N1, H3N2, and influenza B virus isolates also could activate mast cell

208 Forty-nine influenza B virus isolates collected in Belgium, Finland

209 owed moderate antigenic mismatch, and 98% of influenza B virus isolates showed major lineage-level mi

210 d reverse genetics to generate a recombinant influenza B virus lacking the BHA cytoplasmic tail domai

211 Commonly used trivalent vaccines contain one influenza B virus lineage and may be ineffective against

212 While most influenza B virus lineages in Malaysia were short-lived,

213 all 20 known influenza A virus subtypes and influenza B virus lineages.

214 virus subtype H3, likely H3N2 (n = 12), and influenza B virus (n = 18).

215 -CoV-2 (n = 75), influenza A virus (n = 65), influenza B virus (n = 50), or RSV (n = 38) or negative

216 activity comparable to B/Malaysia/2506/2004 influenza B virus NA, making it a bona fide neuraminidas

217 VLPs generated in the absence of the influenza B virus NEP protein were unable to transfer th

218 acid substitutions in the NA glycoprotein of influenza B virus not only can confer antiviral resistan

219 We also provide evidence that influenza B virus NS1 mutants induce a self-adjuvanted i

220 Furthermore, we demonstrate that influenza B virus NS1 protein potently antagonizes human

221 the ISG15 protein: a specific region of the influenza B virus NS1 protein, which includes part of it

222 The fact that influenza A and influenza B virus NS1 proteins bind to NS1-I suggests th

223 orresponding dsRNA binding domain from human influenza B virus NS1B-(15-93).

224 specificity exhibited by the NS1 protein of influenza B virus (NS1B protein).

225 The NS1 protein of influenza B virus (NS1B) specifically binds only human a

226 olates (one RSV, five influenza A virus, two influenza B virus, one parainfluenza virus, and six aden

227 In contrast, infection with influenza B virus or human adenovirus type 5 did not ind

228 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

229 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

230 s, human metapneumovirus, influenza A virus, influenza B virus, parainfluenza viruses 1 to 3, and res

231 3 seasonal virus, influenza A virus H1-2009, influenza B virus, parainfluenza viruses 1 to 4, respira

232 Influenza A virus and influenza B virus particles both contain small integral

233 ly within group 1 and group 2 influenza A or influenza B virus phylogenies.

234 pport the hypothesis that the NS1 protein of influenza B virus plays an important role in antagonizin

235 hemagglutinin (HA) (H1, H2, H3, H5, H7, and influenza B virus) plus neuraminidase (NA) (N1 and N2) r

236 We found that influenza B virus populations have lower within-host gen

237 ransport medium (80 influenza A virus and 16 influenza B virus positive) from both adult and pediatri

238 influenza A/H3 virus-, 30 2009 H1N1-, and 30 influenza B virus-positive specimens and 30 influenza vi

239 Influenza B virus primarily infects humans, causing seas

240 cids 94 to 281), in the absence of any other influenza B virus proteins resulted in the inhibition of

241 a B viruses and (ii) extensive monitoring of influenza B virus reassortants and the mixed genotypes.

242 gglutinin (HA) gene of 57 influenza A and 24 influenza B viruses recovered in a single season were an

243 bodies with high titer HAI titer against all influenza B viruses regardless of pre-immunization histo

244 We studied how the within-host diversity of influenza B virus relates to its global evolution by seq

245 Thus, the NB protein is not essential for influenza B virus replication in cell culture but promot

246 strate that the BM2 protein is essential for influenza B virus replication.

247 virus and 100% and 100% for the detection of influenza B virus, respectively, compared to viral cultu

248 or influenza A virus and 96.0% and 99.9% for influenza B virus, respectively.

249 with H1N1 and H5N1 and with H1N1, H3N2, and influenza B viruses, respectively.

250 In a study of 62 influenza B virus samples from 19 countries, dating from

251 ing influenza A virus packaging signals onto influenza B virus segments, we rescued recombinant influ

252 he Directigen Flu A+B assay detected 9 of 16 influenza B viruses (sensitivity, 56.3%; specificity, 99

253 he INFLU A.B-Quick assay identified 10 of 16 influenza B viruses (sensitivity, 62.5%; specificity, 99

254 tool for user-provided influenza A virus or influenza B virus sequences.

255 Whether influenza B virus shares a similar selective packaging s

256 HPIV2, 5 HPIV3, 3 influenza A virus, and 10 influenza B virus specimens.

257 Influenza B viruses split into 2 distinct lineages in th

258 Cold-adapted (ca) B/Ann Arbor/1/66 is the influenza B virus strain master donor virus for FluMist,

259 es and salivary IgA to influenza A(H3N2) and influenza B virus strains as early as 14 days after vacc

260 ion against both homologous and heterologous influenza B virus strains in the mouse model.

261 Influenza B virus strains in trivalent influenza vaccine

262 -plexed assay for influenza virus typing and influenza B virus sublineage characterization was develo

263 ics system for the generation of recombinant influenza B virus that facilitates the generation of vac

264 r novel vaccine prototype uses an attenuated influenza B virus that has been manipulated to express t

265 e control, while the negative control was an influenza B virus that should not cross-protect against

266 We studied three influenza B viruses that represent both the Yamagata (B/

267 the typing of 179 influenza A viruses and 3 influenza B viruses, the subtyping of 110 H1N1 (S-OIV; N

268 When infected with influenza B virus, these mice cleared the virus in a pro

269 possible explanation for the restriction of influenza B virus to humans.

270 which to study the underlying mechanisms of influenza B virus transmission.

271 e inferred the phylogenetic history of human influenza B virus using complete genome sequences for wh

272 In this study, we report a novel universal influenza B virus vaccination strategy based on "mosaic"

273 ine.IMPORTANCE This work reports a universal influenza B virus vaccination strategy based on focusing

274 e we focus on the development of a universal influenza B virus vaccine based on the lipid nanoparticl

275 lopment of a universal or broadly protective influenza B virus vaccine lags behind the development of

276 nd drive development toward a more effective influenza B virus vaccine.

277 ich could serve as the basis for a universal influenza B virus vaccine.IMPORTANCE This work reports a

278 be used for the generation of high yields of influenza B virus vaccines expressing current HA and NA

279 These studies indicate that influenza B virus variants selected in different host sy

280 icroscopy and immunohistochemical assays for influenza B virus, various bacterial pathogens, and comp

281 namics of the two co-circulating lineages of influenza B virus (Victoria and Yamagata), showing that

282 ynamics of the two cocirculating lineages of influenza B virus, Victoria and Yamagata, are poorly und

283 a A(H3N2) virus, 3.0 [95% CI, 1.8-5.0]), but influenza B virus was not (RR, 1.8; 95% CI, .7-4.6).

284 that the hemagglutinin of Vero cell-derived influenza B viruses was identical to that of MDCK-grown

285 the influenza A, influenza A 2009 H1N1, and influenza B viruses were 99.4%, 98.4%, and 100%, respect

286 influenza A virus subtypes H1N1 and H3N2 and influenza B viruses were detected in 329, 689, and 148 s

287 Conversely, children infected with influenza B viruses were more likely than adults to show

288 is study, we used modified hemagglutinins of influenza B virus which display only one or none of the

289 M2 is a small integral membrane protein from influenza B virus which forms proton-permeable channels.

290 unction of the ISG15 protein is inhibited by influenza B virus, which strongly induces the ISG15 prot

291 Influenza B viruses, which cause a highly contagious res

292 d childhood deaths are due to infection with influenza B viruses, which co-circulate in the human pop

293 ine, whereas no inhibition was observed with influenza B virus, whose NS1B protein lacks a binding si

294 In addition, a recombinant influenza B virus with NS1 deleted induces higher levels

295 Influenza B viruses with a novel I221L substitution in n

296 During 2010-2011, influenza B viruses with a novel neuraminidase substitut

297 re 71.3% for influenza A virus and 93.3% for influenza B virus, with specificities of 100% for both v

298 lineage assignment for 94% of 50 applicable influenza B viruses, with no false assignments.

299 y antigenic analysis of the hemagglutinin of influenza B viruses would fail to detect reassortants.

300 Mismatch between circulating influenza B viruses (Yamagata and Victoria lineages) and