ライフサイエンスコーパス: influenza B

1 were associated with increased incidence of influenza B.

2 d further reduced against lineage-mismatched influenza B.

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

4 entially improving its effectiveness against influenza B.

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

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

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

8 74.4%) were influenza A, and 92 (25.6%) were influenza B.

9 cases of influenza A(H3N2), and 333 cases of influenza B.

10 A(H1N1)pdm09, 408 with A/H3N2, and 199 with influenza B.

11 influenza A (unsubtyped), and 13.3% (n = 50) influenza B.

12 r A(H1N1)pdm09 and 66% (95% CI, 10%-87%) for influenza B.

13 d during periods of increased circulation of influenza B.

14 95% CI, 1.33-2.32) for influenza A(H3N2) and influenza B.

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

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

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

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

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

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

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

22 uenza A (64.6% [CI, 59.0% to 70.1%) than for influenza B (52.2% [CI, 45.0% to 59.3%).

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 In contrast, influenza B activity predominated in colder months throu

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

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

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

29 fections in the study population were due to influenza B and A(H3N2), and influenza A infections were

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

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

32 1N1, and 1 participant was positive for both influenza B and pandemic 2009 H1N1.

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

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

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

36 patients: 4 of 41 with RSV pneumonia, 1 with influenza B, and 1 with MPV/influenza A virus/CoV coinfe

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 75% and 58% for influenza A, 89% and 67% for influenza B, and 93 to 98% and 57% for AdV, respectively

41 .2% (488/492; kappa = 0.94) for influenza A, influenza B, and respiratory syncytial virus, respective

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

43 olymerase chain reaction for influenza A and influenza B, and the viral load (VL) was determined for

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 n HAI titers were similar between groups for influenza B/Brisbane (P = .390).

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

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

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

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

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

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

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

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

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

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

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

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

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

65 crystal structure of hemagglutinin (HA) from influenza B/Hong Kong/8/73 (B/HK) virus determined to 2.

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

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

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

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

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

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

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

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

74 No emergent resistance was found in influenza B infections.

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

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

77 om influenza A/New Caledonia/20/99(H1N1) and influenza B/Jiangsu/10/03 virus and 45 microg of hemaggl

78 e more susceptible to influenza A/WSN/33 and influenza B/Lee/40 virus infections.

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

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

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

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

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

84 hip) designed to detect and identify the two influenza B lineages is presented.

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

86 As a test case, we analyzed influenza B/Malaysia/2506/2004 hemagglutinin, a componen

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

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

89 y distinguishes seasonal A/H1N1 from A/H3N2, influenza B, or 2009 pandemic A/H1N1, making it useful f

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

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

92 NA segment is modified such that it contains influenza B packaging signals, and therefore it cannot b

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

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

95 One-hundred five influenza B-positive specimens obtained from southeast A

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

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

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

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

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

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

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

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

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

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

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

107 rus, three coronavirus, two influenza A, two influenza B, two respiratory syncytial virus, one parain

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

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

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

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

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

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

114 at7e-expressing cells were infected with the Influenza B/Victoria/504/2000 strain.

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

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

117 Influenza B virus (IBV) causes annual influenza epidemic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Influenza B virus causes annual epidemics and, along wit

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

138 Influenza B virus causes significant disease but remains

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 Influenza B virus has been less studied than influenza A

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

155 Influenza B virus hemagglutinin (BHA) contains a predict

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

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

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

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

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

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

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

163 Influenza B virus infection causes rates of hospitalizat

164 18 years; however, the pathogenesis of fatal influenza B virus infection is poorly described.

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

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

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

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

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

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

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

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

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

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

175 Influenza B virus infects only humans and some marine ma

176 Influenza B virus is a human pathogen responsible for si

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 Whether influenza B virus shares a similar selective packaging s

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

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

199 Influenza B virus strains in trivalent influenza vaccine

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

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

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

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

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

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

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

207 0% for influenza A virus, 100% and 99.7% for influenza B virus, and 100% and 100% for respiratory syn

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

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

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

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

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

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

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

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

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

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

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

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

220 3 seasonal virus, influenza A virus H1-2009, influenza B virus, parainfluenza viruses 1 to 4, respira

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

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

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

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

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

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

227 Influenza B virus-induced activation of IRF3 required th

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

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

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

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

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

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

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

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

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

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

240 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

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

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

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

244 Influenza B viruses are important human pathogens that r

245 Influenza B viruses are important human respiratory path

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 Influenza B viruses split into 2 distinct lineages in th

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

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

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

272 Influenza B viruses with a novel I221L substitution in n

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

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

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

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

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

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

279 Influenza B viruses, which cause a highly contagious res

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

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

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

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

284 culating, antigenically distinct lineages of influenza B viruses.

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

286 nces after vaccination were observed against influenza B viruses.

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

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

289 protected from lethal challenge with diverse influenza B viruses.

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

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

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

293 1, 103 seasonal influenza A, and 40 seasonal influenza B) were analyzed.

294 Influenza B Yamagata- and Victoria-lineage viruses have

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

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

297 2 (56%) had influenza A(H3N2), 582 (25%) had influenza B/Yamagata, and 303 (13%) had influenza B/Vict

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

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

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