ライフサイエンスコーパス: influenza B virus

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

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

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

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

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

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

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

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

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

10 pared with controls immunized with unrelated influenza B virus.

11 rom an immunocompromised child infected with influenza B virus.

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

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

14 8% and 98.3% and 100% and 100% for detecting influenza B virus.

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

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

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

18 nces after vaccination were observed against influenza B viruses.

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

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

21 protected from lethal challenge with diverse influenza B viruses.

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

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

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

25 culating, antigenically distinct lineages of influenza B viruses.

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

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

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

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

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

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

32 98%, respectively, but the sensitivities for influenza B virus and adenovirus were unacceptable (14.3

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

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

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

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

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

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

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

40 0% for influenza A virus, 100% and 99.7% for influenza B virus, and 100% and 100% for respiratory syn

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

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

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

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

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

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

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

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

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

50 Influenza B viruses are important human pathogens that r

51 Influenza B viruses are important human respiratory path

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Influenza B virus causes a significant amount of morbidi

66 Influenza B virus causes annual epidemics and, along wit

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

68 Influenza B virus causes significant disease but remains

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Influenza B virus has been less studied than influenza A

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

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

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

98 Influenza B virus hemagglutinin (BHA) contains a predict

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

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

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

102 Influenza B virus (IBV) causes annual influenza epidemic

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

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

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

106 1 strain, the 2009 pandemic H1N1 strain, and influenza B virus in cytotoxicity assays and intracellul

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

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

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

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

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

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

113 Influenza B virus-induced activation of IRF3 required th

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

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

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

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

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

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

120 Influenza B virus infection causes rates of hospitalizat

121 18 years; however, the pathogenesis of fatal influenza B virus infection is poorly described.

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

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

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

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

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

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

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

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

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

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

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

133 Influenza B virus infects only humans and some marine ma

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

135 Influenza B virus is a human pathogen responsible for si

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

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

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

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

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

141 The evolution of influenza B viruses is poorly understood.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

166 0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses (p=0.04).

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

168 3 seasonal virus, influenza A virus H1-2009, influenza B virus, parainfluenza viruses 1 to 4, respira

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 Whether influenza B virus shares a similar selective packaging s

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

188 Influenza B viruses split into 2 distinct lineages in th

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

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

191 Influenza B virus strains in trivalent influenza vaccine

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 Influenza B viruses, which cause a highly contagious res

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

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

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

216 Influenza B viruses with a novel I221L substitution in n

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

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

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

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

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