ライフサイエンスコーパス: human influenza

1 ental model to study viral infections (e.g., human influenza).

2 tiviral and clinical effects in experimental human influenza.

3 n either preventing or treating experimental human influenza.

4 epitope on M2e, was explored in experimental human influenza.

5 emporally and geographically to epidemics of human influenza.

6 plosive epidemic (or pandemic recurrence) of human influenza.

7 en related pathogens including, potentially, human influenzas.

8 of the hemagglutinin of approximately 13,000 human influenza A (H3N2) viruses from six continents dur

9 eviously found in the highly pathogenic (HP) human influenza A (H7N9) [IAV(H7N9)] strains.

10 Human influenza A (subtype H3N2) is characterized geneti

11 are susceptible to infection with avian and human influenza A and B viruses and have been widely use

12 Human influenza A and B viruses infected cells from geog

13 rior adaptation that is usually required for human influenza A H1N1 viruses.

14 e fully susceptible to infection with either human influenza A or B viruses.

15 ge set of available commercial human and non-human influenza A strains were also tested using QIAstat

16 tween 2009 to 2015, for antibodies to eleven human influenza A strains.

17 the HA1 domain of the hemagglutinin genes of human influenza A subtype H3 appear to be under positive

18 Human influenza A virus (IAV) vaccination is limited by

19 /20/99) or an H3 serotype (A/Panama/2007/99) human influenza A virus and then used these constructs a

20 An especially novel aspect of human influenza A virus binding is its ability to equiva

21 The human influenza A virus continues to thrive even among p

22 Although the surface proteins of human influenza A virus evolve rapidly and continually p

23 Here we investigated the replication of human influenza A virus in bat cell lines and the barrie

24 fication of correlates of protection against human influenza A virus infection is important in develo

25 its recognition by the immune system during human influenza A virus infection.

26 the possible roles of anti-M2 antibodies in human influenza A virus infection.

27 y reference strain derived from the earliest human influenza A virus isolate, WS/33.

28 this residue is not conserved in a number of human influenza A virus isolates.

29 n influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, w

30 that phosphorylation of the NS1 protein of a human influenza A virus occurs not only at the threonine

31 To determine the role of MxA in blocking human influenza A virus replication in primate cells, we

32 y of ferrets, a laboratory model species for human influenza A virus research, to vaccine-associated

33 Deep sequencing of adapted human influenza A virus revealed a mutation in the PA po

34 ly, found in the NS1A proteins of almost all human influenza A virus strains.

35 ial cells, the primary cell type infected by human influenza A virus strains.

36 y phosphorylation of the NS1 protein of this human influenza A virus that regulates its replication i

37 We showed that human influenza A virus uses canonical sialic acid recep

38 ts of sequencing 209 complete genomes of the human influenza A virus, encompassing a total of 2,821,1

39 801) elicit robust CTL responses against any human influenza A virus, including H7N9, whereas ethnici

40 ne the extent of homologous recombination in human influenza A virus, we assembled a data set of 13,8

41 for prototypical lab-adapted strains of the human influenza A virus.

42 s only a very minor role in the evolution of human influenza A virus.

43 tification of eight virus species, including human influenza A viruses (i.e., H1N1 and H3N2 strains),

44 determined the genomic make-up of subsequent human influenza A viruses (IAV).

45 mples of such viruses include three pandemic human influenza A viruses and canine parvovirus in dogs.

46 Human influenza A viruses are known to be transmitted vi

47 The NS1A proteins of human influenza A viruses bind CPSF30, a cellular factor

48 The NS1 protein of human influenza A viruses binds the 30-kDa subunit of th

49 it of the RNA polymerase complex of seasonal human influenza A viruses has been shown to localize to

50 Our data suggest that replication of human influenza A viruses in a nonnative host drives the

51 sing the pandemic risk posed by specific non-human influenza A viruses is an important goal in public

52 esults suggest that the currently prevailing human influenza A viruses might have lost their ability

53 Human influenza A viruses preferentially bind alpha2,6-l

54 In seasonal human influenza A viruses, gene segments coevolve at bot

55 as one mechanism for the emergence of novel human influenza A viruses.

56 the relative virulence of selected avian and human influenza A viruses.

57 cid residues that are highly conserved among human influenza A viruses.

58 e and replaced the HA gene of the prevailing human influenza A viruses.

59 ," is virucidal for H1 hemagglutinin-bearing human influenza A viruses.

60 otoxicity was demonstrated against avian and human influenza A viruses.

61 was similar to that of a primary response to human influenza A viruses; serum neutralizing antibody w

62 led PREDAC-H3, for antigenic surveillance of human influenza A(H3N2) virus based on the sequence of s

63 We have studied the HA1 domain of 254 human influenza A(H3N2) virus genes for clues that might

64 thus assisting in antigenic surveillance of human influenza A(H3N2) virus.

65 Our results indicate that the evolution of human influenza A(H3N2) viruses since 1968 has produced

66 circulating pandemic 2009 influenza A(H1N1), human influenza A(H3N2), influenza B, and RSV.

67 A surge of human influenza A(H7N9) cases began in 2016 in China fro

68 imated the incubation period distribution of human influenza A(H7N9) infections using exposure data a

69 Studies reporting serological evidence of human influenza A(H9N2) infection among avian-exposed po

70 We further show that vaccinia virus and human influenza A, B, and C viruses each encode an essen

71 of cytotoxic T lymphocyte escape mutants in human influenza A.

72 sampling bias affect evolutionary studies of human influenza A.

73 Human influenza A/B viruses are unusual in preferring al

74 Hemagglutinin sequences of 146 human influenza A/H3N2 strains identified in respiratory

75 The seasonal human influenza A/H3N2 virus undergoes rapid evolution,

76 Here, we demonstrate that recombinant human influenza A/H3N2 viruses without and with oseltami

77 e determine the structures of FluPol(A) from human influenza A/NT/60/1968 (H3N2) and avian influenza

78 us vaccine produced by truncating NS1 in the human influenza A/Texas/36/91 (H1N1) virus with that of

79 The NS1A protein of the human influenza A/Udorn/72 (Ud) virus inhibits the produ

80 ition to mass vaccination strategies against human influenza, and for the management of antigenically

81 In 1997, 18 confirmed cases of human influenza arising from multiple independent transm

82 Although human influenza B virus (IBV) is a significant human pat

83 the corresponding dsRNA binding domain from human influenza B virus NS1B-(15-93).

84 ions we inferred the phylogenetic history of human influenza B virus using complete genome sequences

85 h less depleted than suggested by a model of human influenza based only on virus-shedding data.

86 Viruses with approximately 50% homology to human influenza C virus (ICV) have recently been isolate

87 revious studies support an increased risk of human influenza cases among individuals with swine conta

88 es (IBV) represent nearly one-quarter of all human influenza cases and are responsible for significan

89 r the 10-year study period, we included 8790 human influenza cases and identified a distinct influenz

90 athological analysis of autopsy samples from human influenza cases from 1918 revealed significant dam

91 on sequencing (NGS) samples generated from a human influenza challenge study wherein 17 healthy subje

92 y and feasibility of aerosol inoculation for human influenza challenge.

93 Studying reassortment patterns of different human influenza datasets, we find large differences in r

94 nship between the degree of inflammation and human influenza disease progression are scarce.

95 ouse experimental model systems for studying human influenza disease.

96 opportunities for more effective control of human influenza epidemics and pandemics by inactivated i

97 model through clinically-relevant, seasonal human influenza examples.

98 ed on the most common avian influenza H5 and human influenza H1 sequences.

99 ) with a genetically reconstructed strain of human influenza H1N1 A/Texas/36/91 virus and hypothesize

100 key/Turkey/1/05) and a moderately pathogenic human influenza H1N1 virus (A/USSR/77), but there were c

101 These results indicate that a human influenza H1N1 virus possessing the 1918 HA and NA

102 In stark contrast to contemporary human influenza H1N1 viruses, the 1918 pandemic virus ha

103 Neuraminidase (NA) of human influenza H3N2 virus has evolved rapidly and been

104 hly homologous to those of highly pathogenic human influenza H5N1 viruses, suggesting that a W312-lik

105 ide synthesis (SPPS) of histidine (His)- and human influenza hemagglutinin (HA)-tags.

106 uenza virus transmission in animal models of human influenza, if not among humans themselves, with im

107 tibodies, but the precise role of T cells in human influenza immunity is uncertain.

108 ons of these results for vaccination against human influenza infection are discussed.

109 Reports of the use of hyperimmune serum in human influenza infection are sporadic and studies in an

110 more pathways relevant to immune-response to human influenza infection than the competing approaches.

111 standard benchmark animal model for studying human influenza infection, in a direct comparison to VAE

112 dered the most reliable animal surrogate for human influenza infection, the newly engineered H5N1 str

113 ge-scale time-course gene expression data on human influenza infection, we demonstrate that our metho

114 Human influenza infections display a strongly seasonal p

115 ts, creating a clinical infection similar to human influenza infections.

116 Human influenza is a highly contagious acute respiratory

117 Human influenza is a seasonal disease associated with si

118 A more cogent model of human influenza is the ferret.

119 accine encoding hemagglutinin from the index human influenza isolate A/HK/156/97 provides immunity ag

120 The threat of pandemic human influenza looms as we survey the ongoing avian inf

121 especially critical determinant of observed human influenza mortality, even after controlling for te

122 e mechanistic insights into the evolution of human influenza NA and elucidate its sequence-structure-

123 ng normal or variant antigenic peptides from human influenza nucleoprotein.

124 Human influenza occurs annually in most temperate climat

125 n Hong Kong raises the possibility of future human influenza outbreaks.

126 raised worldwide concern about an impending human influenza pandemic similar to the notorious H1N1 S

127 Will there be another human influenza pandemic?

128 We find that the four most recent human influenza pandemics (1918, 1957, 1968, and 2009),

129 h airborne transmissibility, suggesting that human influenza pandemics caused by these influenza A(H5

130 oonotic pathogen with the potential to cause human influenza pandemics.

131 1957 (H2N2 subtype) and 1968 (H3N2 subtype) human influenza pandemics.

132 t the clinical relevance of this protease in human influenza pathogenesis.

133 ent in ferrets, the primary animal model for human influenza pathogenesis.

134 In late 2011 and early 2012, 13 cases of human influenza resulted from infection with a novel tri

135 Human influenza-specific TRM isolated from lungs recapit

136 (H1N1), a mouse-adapted virus derived from a human influenza strain first isolated in 1933.

137 and variability in transmissibility of novel human influenza strains as they emerge is a key public h

138 tion with no subtype discrimination, whereas human Influenza strains were positively discriminated.

139 of identified epitopes among avian H5N1 and human influenza strains.

140 d discovered a peptide that destroys diverse human influenza strains.

141 d on antigenic distance and from a published human influenza study.

142 In the case of human influenza, such potential benefits of mass vaccina

143 because the disease state resembles that of human influenza, these animals have been widely used as

144 We used the ferret model of human influenza to systematically investigate viral inte

145 Direct avian-to-human influenza transmission was unknown before 1997.

146 While a tight bottleneck operates in human influenza transmission, it is not extreme in natur

147 The ectodomain of matrix protein 2 (M2e) of human influenza type A virus strains has remained remark

148 previously reported molecular signatures of human influenza vaccination were derived from a single a

149 Most human influenza vaccine antigens are produced in fertili

150 design of optimal immunization regimens for human influenza vaccines, especially for influenza-naive

151 etacoronavirus OC43 (related to SARS-CoV-2), human influenza virus (H1N1), and HSV1 from atomizer-pro

152 nvestigated the role of maternal exposure to human influenza virus [HI] in C57BL/6 mice on day 9 of p

153 d the aerosol transmission efficiencies of 2 human influenza virus A strains and found that A/Panama/

154 hominoids, the hemagglutinin (HA) gene from human influenza virus A, and HIV-1 env, vif, and pol gen

155 very high (>98%) nucleotide homology to the human influenza virus A/Hong Kong/156/97 (H5N1) in the s

156 ge and with geometric mean antibody titer to human influenza virus antigens.

157 C-terminal truncations in the NS1 protein of human influenza virus are sufficient to make the virus a

158 We highlight recent human influenza virus challenge studies that advance our

159 Surveillance for emerging human influenza virus clades is important for identifyin

160 Seasonal human influenza virus continues to cause morbidity and m

161 e polymerase protein sequences from the 1918 human influenza virus differ from avian consensus sequen

162 Human influenza virus evolves to escape neutralization b

163 uenza viruses to rigorously demonstrate that human influenza virus evolves under pressure to fix muta

164 but this effect is less well understood for human influenza virus HA proteins that lack polybasic cl

165 The evolution of human influenza virus haemagglutinin (HA) involves simul

166 considered the 'gold standard' for modeling human influenza virus infection and transmission.

167 ng IFITM3 proteins were involved in blocking human influenza virus infection in endothelial cells.

168 support the premise that a barrier exists to human influenza virus infection in pigs, which may limit

169 We show that human influenza virus infection is blocked during the ea

170 The "gold standard" for serodiagnosis of human influenza virus infection is the detection of sero

171 To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3

172 spiratory death after mouse parainfluenza or human influenza virus infection.

173 anscript changes in blood during symptomatic human influenza virus infection.

174 ated with protection from naturally acquired human influenza virus infections during the 2015-2016 in

175 e of novel pandemic H1N1 as well as seasonal human influenza virus infections in domestic cats in Ohi

176 The serial interval (SI) of human influenza virus infections is often described by a

177 apply this method to an existing data set of human influenza virus infections, showing that transmiss

178 A/NA can play important roles in controlling human influenza virus infectivity in pigs.

179 e dynamics and control, but its relevance to human influenza virus is still unclear.

180 t only markers which are highly preserved in human influenza virus isolates over time.

181 We have previously shown that a recombinant human influenza virus lacking the NS1 gene (delNS1) coul

182 Here, we evaluated a panel of human influenza virus monoclonal antibodies (mAbs) expre

183 virus with 3 A(H1N1)pdm09 genes and a recent human influenza virus N2 gene was transmitted most effic

184 re is clear selection from CD8(+) T cells in human influenza virus NP and illustrates how comparative

185 show that epitope-altering substitutions in human influenza virus NP are enriched on the trunk versu

186 However, even in human influenza virus NP, sites in T-cell epitopes evolv

187 ed the activities of polymerases of avian or human influenza virus origin in pig, human, and avian ce

188 aminidase, and PB1 polymerase genes being of human influenza virus origin, the nucleoprotein, matrix,

189 n early warning of the emergence of the next human influenza virus pandemic.

190 using both the 2009 H1N1 ID kit and the CDC human influenza virus real-time reverse transcription-PC

191 DCK) cell line that expresses high levels of human influenza virus receptors and low levels of avian

192 allow for the recognition of both avian and human influenza virus receptors in the absence of other

193 tently differentiate the 1918 and subsequent human influenza virus sequences from avian virus sequenc

194 ain of the transmembrane matrix 2 protein of human influenza virus stimulated local lymph nodes, incr

195 elated either to avian influenza virus or to human influenza virus strains from Asia from the 1960s,

196 type, subtype, and determine the lineage of human influenza virus strains through the detection of o

197 human endothelial cells limit replication of human influenza virus strains, whereas avian influenza v

198 escribing the phylodynamics of interpandemic human influenza virus subtype A(H3N2).

199 of the RBS naturally varies across avian and human influenza virus subtypes and is also evolvable.

200 The highest titers were observed for human influenza virus subtypes.

201 residues important for NS1 functions and in human influenza virus surveillance to assess mutations a

202 (Mph) demonstrated greater susceptibility to human influenza virus than monocytes, with the majority

203 how that a pH-stable hemagglutinin enables a human influenza virus to replicate more effectively in h

204 r transgenic mouse (2D2) and a mouse-adapted human influenza virus to test the hypothesis that upper-

205 mong sites are used to analyze a data set of human influenza virus type A hemagglutinin (HA) genes.

206 nder clinical development as live attenuated human influenza virus vaccines and induce potent influen

207 The preparation of live, attenuated human influenza virus vaccines and of large quantities o

208 e (both BALB/c and C57BL/6 strains) with the human influenza virus yields offspring that display high

209 ne from A/Texas/36/91 (a seasonal isolate of human influenza virus), as well as the host response to

210 re based on maternal gestational exposure to human influenza virus, the viral mimic polyriboinosinic-

211 a hemagglutinin and neuraminidase from a non-human influenza virus, we assessed which of the three ce

212 Contrary to previous findings with human influenza virus, we found that in the case of equi

213 these vesicles have a neutralizing effect on human influenza virus, which is known to bind sialic aci

214 diversity in recently circulating strains of human influenza virus.

215 a descendant of the 1918 pandemic strain of human influenza virus.

216 ng vessel for generating pandemic strains of human influenza virus.

217 Hemagglutinins (HAs) from human influenza viruses adapt to bind alpha2-6-linked si

218 are naturally susceptible to infection with human influenza viruses and because the disease state re

219 operties that more closely resemble those of human influenza viruses and have the potential to spread

220 y to assess the risks posed to humans by non-human influenza viruses and lead to improved pandemic pr

221 Human influenza viruses and Parvovirus Minute Viruses of

222 ed at least three distinct H3 molecules from human influenza viruses and thus form three distinct phy

223 erally replicate at higher temperatures than human influenza viruses and, although they shared the sa

224 Prototypic receptors for human influenza viruses are N-glycans carrying alpha2,6-

225 Human influenza viruses are proposed to recognize sialic

226 Hemagglutinins (HAs) from human influenza viruses descend from avian progenitors t

227 For example, human influenza viruses do not replicate in duck intesti

228 CIV evolves at a lower rate than H3N2 human influenza viruses do, and viral phylogenies exhibi

229 The hemagglutinin (HA) of H3 human influenza viruses does not support viral replicati

230 n in vivo, we have generated two recombinant human influenza viruses encoding either mitochondrial or

231 inic acid alpha3 (NeuAcalpha3) sugars, while human influenza viruses exhibit a preference for NeuAcal

232 cid, we identified markers that discriminate human influenza viruses from avian influenza viruses.

233 Hemagglutinins (HA's) from duck, swine, and human influenza viruses have previously been shown to pr

234 Our studies with contemporary human influenza viruses identified escape mutants before

235 irus is compatible for genetic exchange with human influenza viruses in human cells, suggesting the p

236 analyses of PA-X substitutions conserved in human influenza viruses indicated that R195K, K206R, and

237 Although we found that human influenza viruses infected both ciliated and nonci

238 uried surface of the complex have mutated in human influenza viruses isolated after 1998, confirming

239 In particular, the PB2 proteins of seasonal human influenza viruses localize to the mitochondria whi

240 signed to cross-react with avian, swine, and human influenza viruses of the N1 NA subtype.

241 clear whether prior exposure to circulating human influenza viruses or influenza vaccination confers

242 H5) influenza viruses, we observed that the human influenza viruses primarily infected ciliated cell

243 termines resistance of seasonal and pandemic human influenza viruses to Mx, while avian isolates reta

244 genes via reassortment and the adaptation of human influenza viruses to new swine hosts.

245 In HULEC, human influenza viruses were capable of binding to host

246 assays of viral traits to identify those non-human influenza viruses with the greatest risk of evolvi

247 ing specificity with Asp (typically found in human influenza viruses) and Gly (typically found in avi

248 se they possess receptors for both avian and human influenza viruses, and emergence may occur in sout

249 antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF

250 e susceptible to infection by both avian and human influenza viruses, and this feature is thought to

251 H3 and N1 and N2 antigens have been found in human influenza viruses, but virologic history is too br

252 e-based assays for susceptibility testing of human influenza viruses, detection of DeltaRNA segments

253 Like human influenza viruses, EIV H3N8 caused a transcontinen

254 triple reassortant between avian, swine, and human influenza viruses, highlighting the importance of

255 endothelium possesses intrinsic immunity to human influenza viruses, in part due to the constitutive

256 t guinea pigs can be infected with avian and human influenza viruses, resulting in high titers of vir

257 an intermediate host in the emergence of new human influenza viruses, there is still little known abo

258 st studies have focused on NAI-resistance in human influenza viruses, we investigated the molecular c

259 infection, replication, and spread of seven human influenza viruses.

260 els are substantially different in swine and human influenza viruses.

261 r pigs as possible adaptation hosts of novel human influenza viruses.

262 ot cross-react with HAs of more contemporary human influenza viruses.

263 ceptibility to infection with both avian and human influenza viruses.

264 binding molecules preferred by the avian and human influenza viruses.

265 infection, a specificity also described for human influenza viruses.

266 ely resistant to experimental infection with human Influenza viruses.

267 stantial portion of the circulating seasonal human influenza viruses.

268 pH for hemagglutinin activation, similar to human influenza viruses.

269 se of their susceptibility to both avian and human influenza viruses.

270 s reassortment between prepandemic avian and human influenza viruses.

271 ent positively contributes to the fitness of human influenza viruses.

272 e that had been previously immunized against human influenza viruses.

273 e spatio-temporal incidence and evolution of human influenza viruses.

274 ences in reassortment rates across different human influenza viruses.

275 t two species are well-established models of human influenza, while swine are a natural host and a fr