ライフサイエンスコーパス: influenza B

1 =65 years) and type/subtype (A/H1N1, A/H3N2, influenza B).

2 e enrolled 170 children (127 influenza A, 43 influenza B).

3 95% CI, 1.33-2.32) for influenza A(H3N2) and influenza B.

4 za A(H3N2) but not influenza A(H1N1)pdm09 or influenza B.

5 ositive: 590 (72%) influenza A and 226 (28%) influenza B.

6 enza A/H3N2 virus but were effective against influenza B.

7 were associated with increased incidence of influenza B.

8 d further reduced against lineage-mismatched influenza B.

9 H1N1; 335 H3N2; 899 H1N1pdm2009) and 518 had influenza B.

10 entially improving its effectiveness against influenza B.

11 nza A, but an improved virologic response in influenza B.

12 s, 54 (95%) were influenza A and 3 (5%) were influenza B.

13 than in adults and for influenza A than for influenza B.

14 74.4%) were influenza A, and 92 (25.6%) were influenza B.

15 d quadrivalent vaccines in preventing severe influenza B.

16 1N1)pdm09, and 50% (95% CI, 41%-57%) against influenza B.

17 40) and 10 (95% CI, 7-15), respectively; and influenza B, 26 (95% CI, 19-35) and 14 (95% CI, 11-18),

18 1) and 14 (95% CI, 11-18), respectively; and influenza B, 26 (95% CI, 21-32) and 17 (95% CI, 14-22),

19 nfluenza A(H1N1)pdm09 (3.1 days), the SI for influenza B (3.7 days) was 22% longer (95% confidence in

20 of participants had confirmed infection with influenza B, 33% with seasonal H3N2, 29% with pandemic 2

21 he HD than SD vaccine after stimulation with influenza B (367 vs 0; P = .002).

22 ulated; VE was statistically significant for influenza B (63.0%; 95% CI, 24.2%-83.7%) but not influen

23 us, predominantly for A(H1N1)pdm09 (11%) and influenza B (7%).

24 -3 to 10 percentage points]; P = 0.32), and influenza B (91% vs. 80%; treatment difference, 11 perce

25 2 (54 of 118 [46%, 36.6-55.2]; p<0.0001) and influenza B (95 of 118 [81%, 72.2-87.2]; p<0.0001), alon

26 In contrast, influenza B activity predominated in colder months throu

27 Due to the low prevalence of influenza B, an additional 40 banked influenza B-positiv

28 y titer geometric mean fold increase against influenza B and (2) lower seroconversion rates against i

29 bsolute) per month for influenza A(H3N2) and influenza B and 6% - 11% per month for influenza A(H1N1)

30 Patients admitted to hospital with influenza B and A in Jerusalem, Israel, during the 2015-

31 st six months for influenza A(H1N1)pdm09 and influenza B and at least five months for influenza A(H3N

32 esicular stomatitis virus expressing OVA and influenza B and increased numbers of virus-specific CD8

33 1N1, and 1 participant was positive for both influenza B and pandemic 2009 H1N1.

34 ed with mortality in all studied age groups; influenza B and parainfluenza were additionally associat

35 virus [RSV], 120 for influenza A, and 33 for influenza B) and 246 were negative.

36 east 1 virus (13 rhinovirus, 3 adenovirus, 2 influenza B, and 1 enterovirus), which was also signific

37 f 181 cases of influenza A/H3N2, 47 cases of influenza B, and 6 cases of nonsubtypeable influenza A w

38 mples, 958 (77%) were influenza A, 268 (22%) influenza B, and 7 (1%) influenza type C; of influenza A

39 h LDTs were 97.8% for influenza A, 97.2% for influenza B, and 89.3% for RSV.

40 ss (mOR: 3.7, 95% CI: 2.0, 6.9), followed by influenza B, and A(H3N2).

41 ug-resistant influenza A strains, as well as influenza B, and improved survival of influenza-infected

42 .2% (488/492; kappa = 0.94) for influenza A, influenza B, and respiratory syncytial virus, respective

43 stic assay for the detection of influenza A, influenza B, and RSV.

44 rivalent influenza vaccines (TIVs) contain 1 influenza B antigen, meaning lineage mismatch with the v

45 H1N1, 93% (89%) for H3N2, and 53% (68%) for influenza B at 1-3 week leads.

46 fluenza viruses (influenza A H1N1, H3N2, and influenza B) at the same time in 20min and therefore has

47 n = 1817), and 395 (4.2%) were positive for influenza B (B/Yamagata, n = 340).

48 The M2 protein of influenza B (BM2) forms a tetrameric proton-conducting c

49 The M2 protein of influenza B (BM2) is a membrane-embedded tetrameric prot

50 The PB1 subunit of the influenza B/Brisbane/60/2008 strain was used to incorpor

51 he antibody responses to the fourth antigen, influenza B/Brisbane/60/2008, were low in each group, ma

52 ccination reduced the likelihood of shedding influenza B but not (H1N1)pdm09.

53 distance from Mexico and the proportions of influenza B cases among the countries during the post-pa

54 The proportions of influenza B cases displayed wide variations over the stu

55 ly, in the United States, the proportions of influenza B cases in the pre-pandemic period (2003-2008)

56 atio-temporal patterns of the proportions of influenza B cases out of all typed cases, with data from

57 ributed to successful circulation of diverse influenza B clades.

58 received TIV had a reduced risk of seasonal influenza B confirmed by RT-PCR, with a vaccine efficacy

59 t of vaccine mismatch on the epidemiology of influenza B during 12 recent seasonal outbreaks of influ

60 One patient died from influenza B encephalitis during an endemic outbreak 10 m

61 receive influenza vaccine or placebo, for an influenza B epidemic in Hong Kong.

62 Influenza A H3N2, pandemic H1N1, and influenza B equally co-circulated in the first post-pand

63 w factors that are important determinants of influenza B evolution and epidemiology.

64 uding an assay for influenza A (FluA) virus, influenza B (FluB) virus, and respiratory syncytial viru

65 ism is common to both influenza A (FluA) and influenza B (FluB) viruses, FluB PB2 recognizes a wider

66 Influenza A accounted for 74.0% and influenza B for 26.0% of all typed viruses.

67 Seroprotection rates for influenza B, H1N1, and H3N2 were not different (1) betwe

68 conserved epitopes in the head region of the influenza B hemagglutinin (HA), whereas CR9114 binds a c

69 Recombinant mosaic influenza B hemagglutinin proteins and recombinant virus

70 Influenza A (IAV) and influenza B (IBV) viruses are highly contagious pathogen

71 Most (63%) influenza B ICU patients received influenza B-mismatched

72 IgG was significantly lower among women with influenza B illness (93.9 AU/mL) than among their counte

73 gG were significantly lower among women with influenza B-illness (93.9 AU/ml) than their counter-part

74 , seasonal influenza A(H1N1) in 7 (28%), and influenza B in 2 (8%), and in 2 years multiple types coc

75 in 21 (81%; 20 of which [95%] were H1N1) and influenza B in 4 (15%).

76 e sequence data describing a chronic case of influenza B in a severely immunocompromised child we inf

77 QIV may offer improved protection against influenza B in children compared with current trivalent

78 rgan subgroups had higher response rates for influenza B in the ID vaccine group.

79 nfluenza A(H3N2), 648 (9%) were positive for influenza B (including B/Yamagata, n = 577), and 5040 (7

80 vipiravir and zanamivir successfully cleared influenza B infection in a child who had undergone bone

81 Enhanced resistance upon influenza B infection in USP18(C61A/C61A) mice was compl

82 ath (treatment-unrelated encephalitis due to influenza B infection), one life-threatening pyrexia, an

83 In contrast, for influenza B infection, a 10-fold increase in the abundan

84 By contrast, for influenza B infection, a 10-fold increase in the abundan

85 TIV prevented pandemic influenza A(H1N1) and influenza B infections in children.

86 e estimated that 41.7% (3750 of 8993) of all influenza B infections were caused by viruses representi

87 No emergent resistance was found in influenza B infections.

88 .59) and was 3.19 (1.21-8.42) for those with influenza B (interaction p=0.023).

89 We challenge the notion that influenza B is milder than influenza A by finding simila

90 clinical benefit of hIVIG for patients with influenza B is supported by antibody affinity analyses,

91 resenting one H1N1, one H3N2, and one to two influenza B isolates, are selected for inclusion in the

92 Age-related differences in influenza B lineage detection were explored in the commu

93 was cocirculation of influenza A(H3N2) and 2 influenza B lineage viruses in the United States.

94 gnificant difference in clinical severity by influenza B lineage, with the exceptions that (i) the Ya

95 Two antigenically distinct influenza B lineages have cocirculated since 2001, yet t

96 ide strong support for the inclusion of both influenza B lineages in seasonal influenza vaccines.

97 omplex epidemiological dynamics of different influenza B lineages within a single geographic locality

98 The influenza B M2 (BM2) proton channel is activated by acid

99 describe Fc mutants that potently disrupted influenza B-mediated agglutination of human erythrocytes

100 Most (63%) influenza B ICU patients received influenza B-mismatched trivalent vaccine.

101 onitor and develop robust protection against influenza B morbidity and mortality.

102 ve site of influenza A N1-N9 NA subtypes and influenza B NA differs substantially.

103 rols, although this reached significance for influenza B only.

104 No patient tested positive for influenza A, influenza B, or other respiratory viruses.

105 vs 45.5% for A(H3N2); and 83.4% vs 71.8% for influenza B (P < .05).

106 for influenza A(H3N2); and 90.7% vs 75% for influenza B; P < .05).

107 Besides influenza A and RSV, influenza B, parainfluenza and norovirus may also contri

108 A H1, influenza A H3, influenza A H1N1/2009, influenza B, parainfluenza virus 1, parainfluenza virus

109 Subanalysis of influenza B patients showed faster RNA decline rate (ana

110 ect on mortality was observed for A/H1N1 and influenza B patients.

111 ence of influenza B, an additional 40 banked influenza B-positive specimens were tested at the partic

112 ng, there were 1,666 and 274 influenza A and influenza B positives, respectively, across the 2018 to

113 a season and 1,857 and 1,449 influenza A and influenza B positives, respectively, during the 2019 to

114 of both a replication-competent fluorescent influenza B reporter virus and bioluminescent influenza

115 nfluenza B reporter virus and bioluminescent influenza B reporter virus.

116 A, respectively, and of 91.8% and 53.6% for influenza B, respectively.

117 types A(H1N1), A(H3N2), and A(H1N1)pdm09 and influenza B, respectively.

118 n circulation-influenza A (season-specific), influenza B, respiratory syncytial virus (RSV), parainfl

119 eeded to understand age-related variation in influenza B risk by lineage, with potential implications

120 for influenza A/H1N1, influenza A/H3N2, and influenza B strains.

121 diatric-specific data; 35 influenza A and 16 influenza B studies presented adult-specific data.

122 Forty-six influenza A and 24 influenza B studies presented pediatric-specific data; 3

123 l-conserved A(H1N1)pdm09 and lineage-matched influenza B, suboptimal against genetic-variants of A/H3

124 H3N2 and influenza B titers were similar between seasons.

125 res against influenza A and smaller rises in influenza B titres.

126 A(H1N1)pdm09 (VE, 68%; 95% CI, 19%-87%) and influenza B (VE, 48%; 95% CI, 1%-73%).

127 virus (A[H1N1]pdm09) epidemic and concurrent influenza B(Victoria) virus activity.

128 In this influenza B-Victoria and A(H1N1)-dominated season, RIV4

129 nsity and dilution of chemically inactivated influenza B/Victoria and influenza B/Yamagata.

130 imental conditions, with transmissibility of influenza B/Victoria lineage virus among pigs being obse

131 had influenza B/Yamagata, and 303 (13%) had influenza B/Victoria.

132 lineage), and 51% (95% CI, 36%-63%) against influenza B/Victoria.

133 uenza A(H1N1) and vaccine lineage-mismatched influenza B/Victoria; the VE for fully vaccinated childr

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

135 Influenza B virus (IBV) causes annual influenza epidemic

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

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

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

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

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

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

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

143 Influenza B virus (IBV) undergoes seasonal antigenic dri

144 1 influenza A virus (IAV), group 2 IAV, and influenza B virus (IBV) were designed and produced in ba

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

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

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

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

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

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

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

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

153 Influenza B virus causes annual epidemics and, along wit

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

155 Influenza B virus causes significant disease but remains

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

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

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

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

160 Influenza B virus evolves more slowly than influenza A v

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

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

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

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

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

166 Influenza B virus has been less studied than influenza A

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

168 The influenza B virus hemagglutinin contains four major anti

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

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

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

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

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

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

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

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

177 Influenza B virus infection causes rates of hospitalizat

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

179 18 years; however, the pathogenesis of fatal influenza B virus infection is poorly described.

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

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

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

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

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

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

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

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

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

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

190 Influenza B virus infects only humans and some marine ma

191 Influenza B virus is a human pathogen responsible for si

192 Influenza B virus is a serious health concern for childr

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

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

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

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

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

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

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

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

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

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

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

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

205 Whether influenza B virus shares a similar selective packaging s

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

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

208 Influenza B virus strains in trivalent influenza vaccine

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

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

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

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

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

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

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

216 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).

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

218 0% for influenza A virus, 100% and 99.7% for influenza B virus, and 100% and 100% for respiratory syn

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

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

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

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

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

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

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

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

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

228 Influenza B virus-induced activation of IRF3 required th

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

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

231 8% and 98.3% and 100% and 100% for detecting influenza B virus.

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

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

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

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

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

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

238 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

239 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

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

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

242 Influenza B viruses are important human pathogens that r

243 Influenza B viruses are important human respiratory path

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

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

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

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

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

249 Influenza B viruses cause seasonal epidemics and are a c

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

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

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

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

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

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

256 Influenza B viruses have circulated in humans for over 8

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

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

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

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

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

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

263 Influenza B viruses split into 2 distinct lineages in th

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

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

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

267 Influenza B viruses with a novel I221L substitution in n

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

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

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

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

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

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

274 protected from lethal challenge with diverse influenza B viruses.

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

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

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

278 culating, antigenically distinct lineages of influenza B viruses.

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

280 inhibition assay and microneutralisation for influenza B viruses.

281 ilable for antibodies that broadly recognize influenza B viruses.

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

283 s (14% vs 4%; P < .001) and among those with influenza B vs A(H3N2) virus infections (7% vs 0.3%; P <

284 Total vaccine efficacy against influenza B was 32.5% (11.3-48.6) in year 1, 4.9% (-38.9

285 VE against influenza B was 51% (95% CI, 26%-67%) in total: 71% (95%

286 Vaccine effectiveness (VE) against influenza B was derived separately for Victoria and Yama

287 Influenza B was detected in 34.1% with influenza A/H1N1

288 g data from samples from 91 individuals with influenza B, we find that IBV accumulates lower genetic

289 influenza A and 92.9/96.7 and 78.6/98.7 for influenza B were obtained for the Sofia and Veritor assa

290 fluenza (683, A/H1N1pdm09; 825, A/H3N2; 623, influenza B) were investigated.

291 influenza (683 A/H1N1pdm09; 825 A/H3N2; 623 influenza B) were investigated.

292 Influenza B Yamagata- and Victoria-lineage viruses have

293 VE against influenza B(Yamagata) was 57% (95% CI: -3%, 82%) but onl

294 uenza A(H3N2), 66% (95% CI, 58%-73%) against influenza B/Yamagata (vaccine lineage), and 51% (95% CI,

295 fluenza A(H3N2), H1N1 and lineage-mismatched influenza B/Yamagata cocirculated; VE was statistically

296 2 (56%) had influenza A(H3N2), 582 (25%) had influenza B/Yamagata, and 303 (13%) had influenza B/Vict

297 not statistically significant, unlike VE for influenza B/Yamagata, which was 55% (95%CI, 43% to 65%).

298 mically inactivated influenza B/Victoria and influenza B/Yamagata.

299 or H3N2 (all p>0.05) and 78.8% and 97.1% for influenza-B/Yamagata (p=0.03), respectively.

300 chial epithelial (NHBE) cells of recombinant influenza B/Yamanashi/166/1998 viruses containing a sing