ライフサイエンスコーパス: influenza A virus

1 isolate human platelets and treat them with influenza A virus.

2 t transmission bottleneck similar to that of influenza A virus.

3 disease following respiratory challenge with influenza A virus.

4 behind the development of such a vaccine for influenza A virus.

5 oss-protection between different subtypes of influenza A virus.

6 (TLR4, TLR1/2, and TLR7/8) or infection with influenza A virus.

7 le East respiratory syndrome coronavirus and influenza A virus.

8 , agglutinates erythrocytes, and neutralizes influenza A virus.

9 icular, yet remains understudied compared to influenza A virus.

10 rototypical lab-adapted strains of the human influenza A virus.

11 n and reduced its antiviral activity against Influenza A virus.

12 iral genome transcription and replication in influenza A virus.

13 of successful cross-species transmission of influenza A viruses.

14 , as they are in the HA protein of mammalian influenza A viruses.

15 smissibility, and interspecies adaptation of influenza A viruses.

16 was phylogenetically distinct from all other influenza A viruses.

17 sponse to infection of different subtypes of influenza A viruses.

18 targeting the hemagglutinin stalk of group 1 influenza A viruses.

19 indicate that bats may harbor a diversity of influenza A viruses.

20 utinin (HA) head domain and reacts with most influenza A viruses.

21 R) is an essential entry determinant for bat influenza A viruses.

22 mechanisms distinct from those of classical influenza A viruses.

23 odel (Tempel) for the mutation prediction of influenza A viruses.

24 nique among CoVs, but reminiscent of that of influenza A viruses.

25 ers against different clades of H1N1 subtype influenza A viruses.

26 by BFPP were rhinovirus/enterovirus (4.5%), influenza A virus (3%), and respiratory syncytial virus

27 s were detected in 49 children infected with influenza A virus (34 A/H1N1pdm09; 15 A/H3N2) treated wi

28 s were detected in 49 children infected with influenza A virus (34, A/H1N1pdm09; 15, A/H3N2) treated

29 onger times, this "low-fidelity" assembly of influenza A virus allows small populations to survive en

30 ss these questions by developing a strain of influenza A virus amenable to rapid compositional charac

31 ave lower within-host genetic diversity than influenza A virus and experience a tight genetic bottlen

32 an cells using Chikungunya virus (CHIKV) and influenza A virus and identified hundreds of direct RNA-

33 Aspergillus fumigatus were co-infected with influenza A virus and Streptococcus pneumoniae seven day

34 s platform using different subtypes of avian influenza A viruses and human samples with respiratory i

35 ses, including human immunodeficiency virus, influenza A virus, and yellow fever virus.

36 ed by haemagglutination inhibition assay for influenza A viruses, and by hemagglutination inhibition

37 Seasonal outbreaks of influenza A virus are a major cause of illness and death

38 These findings indicate that LP avian H7 influenza A viruses are able to infect and cause disease

39 Human influenza A viruses are known to be transmitted via the

40 Influenza A viruses are responsible for seasonal epidemi

41 c mice were infected with a low dose of H1N1 influenza A virus at gestation day 9.5.

42 e processes have recently been described for influenza A virus, but little is known about the evoluti

43 Influenza B virus evolves more slowly than influenza A virus, but the factors underlying this are n

44 es seasonal antigenic drift more slowly than influenza A virus, but the reasons for this difference a

45 rds are believed to be the reservoir for all influenza A viruses, but this has recently been challeng

46 that sequential infection with the identical influenza A virus can occur and suggest it may not be ra

47 Pandemic influenza A viruses can emerge from swine, an intermedia

48 ent a vast reservoir from which new pandemic influenza A viruses can emerge(1).

49 Influenza A virus carries hundreds of trimeric hemagglut

50 t, as more than 95% of currently circulating influenza A viruses carry this mutation.

51 Influenza A viruses cause pandemics when they cross betw

52 Influenza A viruses cause widespread human respiratory d

53 Influenza A virus causes annual epidemics in humans and

54 Influenza A virus causes millions of severe cases of dis

55 vaccines can provide protection against any influenza A virus challenge.

56 modulating IFN responses.IMPORTANCE Diverse influenza A viruses circulate in wild aquatic birds, occ

57 Influenza A viruses contain a segmented negative-sense R

58 Influenza A viruses continue to circulate among wild bir

59 The influenza A virus deploys this strategy to bind strongly

60 mental infections with different subtypes of influenza A virus derived from different hosts, we found

61 responses in mice to two naturally presented influenza A virus-derived peptides previously identified

62 netic diversity than previously observed for influenza A virus during acute infections.

63 7-labeled full length M2 (M2FL) protein from Influenza A virus embedded in synthetic liquid crystalli

64 H3N2 strains of influenza A virus emerged in humans in 1968 and have con

65 gglutinin-like H18 protein of the bat H18N11 influenza A virus, enabling tropism of the viruses in a

66 bosome, play opposite roles in generating an influenza A virus-encoded peptide.

67 The major bat influenza A virus envelope glycoprotein, haemagglutinin,

68 Influenza A viruses evolve rapidly to escape host immuni

69 as both HuMxA and MuMx1 are antiviral toward influenza A virus (FLUAV) (an orthomyxovirus), only HuMx

70 RNA polymerases of avian influenza A viruses (FluPolA) replicate viral RNA ineffi

71 rveillance, we isolated and characterized an influenza A virus from Egyptian fruit bats.

72 ely, our data indicate that packaging of the influenza A virus genome is controlled by a redundant an

73 and the two principal spike proteins of the influenza A virus (H3N2): hemagglutinin (H3) and neurami

74 onally uncharacterized plasticity of the bat influenza A virus haemagglutinin means the tropism and z

75 lution crystal structure of FluPol(A) of bat influenza A virus has previously been reported(6), there

76 The PA-X protein of influenza A virus has roles in host cell shutoff and vir

77 a vaccines against the conserved epitopes of influenza A virus have been proposed to minimize the bur

78 Influenza A viruses have regularly jumped to new host sp

79 s and tropism.IMPORTANCE Many zoonotic avian influenza A viruses have successfully crossed the specie

80 ly protective, stem-targeted Abs against the influenza A virus hemagglutinin (HA) have been well stud

81 le broadly protective antibodies against the influenza A virus hemagglutinin have been well studied,

82 ghly specific as multiple viruses, including influenza A virus, HIV-1, Rift Valley fever virus, and d

83 k representing the healthy cell state and an influenza A virus-host network representing the infected

84 in laboratory mice, but very few in natural influenza A virus hosts, have demonstrated that M2e-base

85 Influenza A virus (IAV) activates ZBP1-initiated RIPK3-d

86 nfection of human lung epithelial cells with influenza A virus (IAV) also induces a broad program of

87 proteins including HIV, Ebola virus (EBOV), influenza A virus (IAV) and Epstein Barr virus (EBV).

88 t the transmembrane protease TMPRSS2 cleaves influenza A virus (IAV) and influenza B virus (IBV) HA p

89 essential host factors for mammalian-adapted influenza A virus (IAV) and influenza B virus (IBV) repl

90 s of many highly pathogenic RNA viruses like influenza A virus (IAV) and Lassa virus depends on host

91 al genetic interaction between proteins from influenza A virus (IAV) and Middle East respiratory synd

92 Recognition of influenza A virus (IAV) by the innate immune system trig

93 o treat other pathogen infections.IMPORTANCE Influenza A virus (IAV) causes a human respiratory disea

94 Influenza A virus (IAV) causes a wide range of extraresp

95 Influenza A virus (IAV) causes severe respiratory infect

96 Influenza A virus (IAV) causes significant morbidity and

97 therapy, and basic virus research.IMPORTANCE Influenza A virus (IAV) causes significant morbidity and

98 ng pneumonia, with greater health risks upon influenza A virus (IAV) co-infection.

99 o noninvasively detect and quantify airborne influenza A virus (IAV) densities in a public elementary

100 Influenza A virus (IAV) effectively manipulates host mac

101 Influenza A virus (IAV) enters cells by binding to siali

102 id composition influences many stages of the influenza A virus (IAV) entry process, including initial

103 merits further study.IMPORTANCE The varying influenza A virus (IAV) exposure and infection status of

104 Replication of influenza A virus (IAV) from negative-sense viral RNA (v

105 erged lineage of human-like H3N2 (H3.2010.1) influenza A virus (IAV) from swine has been frequently d

106 The incoming influenza A virus (IAV) genome must pass through two dis

107 We combined conventional surveillance with influenza A virus (IAV) genome sequencing to identify an

108 Influenza A virus (IAV) has a segmented genome, which (i

109 sis of respiratory syncytial virus (RSV) and influenza A virus (IAV) have been linked to TLR4 activat

110 09) was first identified as a novel pandemic influenza A virus (IAV) in 2009.

111 grade RNA from SARS-CoV-2 sequences and live influenza A virus (IAV) in human lung epithelial cells.

112 Influenza A virus (IAV) increases the presentation of cl

113 Influenza A virus (IAV) infection constitutes an annual

114 Influenza A virus (IAV) infection during pregnancy cause

115 d the AHR impairs CD4(+) T cell responses to influenza A virus (IAV) infection in adulthood.

116 st-cell-based assay to probe glycan-mediated influenza A virus (IAV) infection including wild-type an

117 o other treatments.IMPORTANCE Infection with influenza A virus (IAV) infection is responsible for an

118 ze readthrough transcription observed during influenza A virus (IAV) infection, validating its specif

119 determine the effect of Sia modifications on influenza A virus (IAV) infection, we tested for effects

120 astically enhanced host resistance to severe influenza A virus (IAV) infection.

121 4 transcription factors in AM in response to influenza A virus (IAV) infection.

122 surfaces and has therapeutic benefit against influenza A virus (IAV) infection.

123 ys an essential role in host defense against influenza A virus (IAV) infection.

124 pact on host-to-host transmission.IMPORTANCE Influenza A virus (IAV) infections are important threats

125 during influenza virus infection.IMPORTANCE Influenza A virus (IAV) infections cause seasonal and pa

126 al models (MMs) have described the course of influenza A virus (IAV) infections in vivo, none have co

127 The influenza A virus (IAV) is a continuous health threat to

128 Influenza A virus (IAV) is a human respiratory pathogen

129 Influenza A virus (IAV) is a lytic RNA virus that trigge

130 Influenza A virus (IAV) is a major public health problem

131 ponses at inhibiting virus spread.IMPORTANCE Influenza A virus (IAV) is a respiratory pathogen of hig

132 Infection with a single influenza A virus (IAV) is only rarely sufficient to ini

133 The viral ribonucleoprotein (vRNP) of the influenza A virus (IAV) is responsible for the viral RNA

134 In contrast, reinfection by influenza A virus (IAV) largely requires antigenic chang

135 hese prototypic adamantane inhibitors of the influenza A virus (IAV) M2 proton channel, a growing num

136 ee of conservation of CD8 T cell epitopes of influenza A virus (IAV) may allow for the development of

137 The influenza A virus (IAV) nonstructural protein 1 (NS1) co

138 Influenza A virus (IAV) nonstructural protein 1 (NS1), a

139 2009 to 2018, of whom 8011 were positive for influenza A virus (IAV) or influenza B virus (IBV).

140 tion.IMPORTANCE The inflammatory response to influenza A virus (IAV) participates in infection contro

141 The evolutionarily conserved influenza A virus (IAV) protein PA-X has been implicated

142 Influenza A virus (IAV) remains a global health concern

143 Despite the cytopathic nature of influenza A virus (IAV) replication, we recently reporte

144 In contrast, reinfection by influenza A virus (IAV) requires antigenic change.

145 Studying influenza A virus (IAV) requires the use of secondary ap

146 Sequence analyses of the influenza A virus (IAV) surface antigen neuraminidase (N

147 Influenza A virus (IAV) utilizes multiple strategies to

148 Early interactions of influenza A virus (IAV) with respiratory epithelium migh

149 Influenza A virus (IAV), a major cause of human morbidit

150 The influenza A virus (IAV), a respiratory pathogen for huma

151 ficities such as Herpes Simplex Virus (HSV), Influenza A Virus (IAV), and Merkel Cell Polyomavirus (M

152 acrophages in the lung detect and respond to influenza A virus (IAV), determining the nature of the i

153 ensus hemagglutinin (cHA) stalks for group 1 influenza A virus (IAV), group 2 IAV, and influenza B vi

154 tinin (HA), a glycoprotein on the surface of influenza A virus (IAV), initiates the virus life cycle

155 For enveloped viruses, such as the influenza A virus (IAV), large N-linked glycans can also

156 V were impaired in their restriction of H5N1 influenza A virus (IAV), other super-restrictor variants

157 With the current knowledge of influenza A virus (IAV), we designed a nanoparticle-base

158 ngs are recognized by many pathogens such as influenza A virus (IAV), yet little is known about their

159 ntify and quantify 21 class 1 MHC-restricted influenza A virus (IAV)-peptides following either direct

160 Influenza A virus (IAV)-related mortality is often due t

161 ol consumption has detailed that the primary influenza A virus (IAV)-specific CD8 T cell response in

162 Influenza A virus (IAV)-specific T cell responses are im

163 injury, and mortality in mice infected with influenza A virus (IAV).

164 ncoded by the +1 register of NS1 mRNA in the influenza A virus (IAV).

165 inhibitors of the adhesion protein HA of the influenza A virus (IAV).

166 re vital for heterologous protection against influenza A virus (IAV).

167 : lymphocytic choriomeningitis virus (LCMV); influenza A virus (IAV); and vesicular stomatitis virus

168 ugs to treat influenza infections.IMPORTANCE Influenza A viruses (IAV) and influenza B viruses (IBV)

169 Influenza A viruses (IAV) are known to modulate and "hij

170 Influenza A viruses (IAV) are lytic viruses that have re

171 Influenza A viruses (IAV) are subject to species barrier

172 rform efficient viral replication.IMPORTANCE Influenza A viruses (IAV) constitute a major public heal

173 Assembly of infectious influenza A viruses (IAV) is a complex process involving

174 Influenza A viruses (IAV) sporadically transmit from swi

175 inical effectiveness against IBV compared to influenza A viruses (IAV).

176 , Sindbis virus [SV], rabies virus [RV], and influenza A virus [IAV]) remains detectable in the mouse

177 c birds are the primary natural reservoir of influenza A viruses (IAVs) and are therefore responsible

178 Influenza A viruses (IAVs) cause more than 2 million ann

179 se induced by avian IAV in humans.IMPORTANCE Influenza A viruses (IAVs) cause seasonal epidemics whic

180 ral fairs are exposed to genetically diverse influenza A viruses (IAVs) circulating in exhibition swi

181 Influenza A viruses (IAVs) constitute a major threat to

182 976 of waterfowl as the primary reservoir of influenza A viruses (IAVs) has since spurred decades of

183 Subtype H10 influenza A viruses (IAVs) have been recovered from dome

184 nza outbreaks of 1918 and 2009, subtype H1N1 influenza A viruses (IAVs) have caused seasonal epidemic

185 ld be continued.IMPORTANCE Subtype H10 avian influenza A viruses (IAVs) have caused sporadic human in

186 Influenza A viruses (IAVs) have caused worldwide epidemi

187 Novel H1N2 influenza A viruses (IAVs) in swine have been identified

188 Avian influenza A viruses (IAVs) naturally infect different av

189 Influenza A viruses (IAVs) quickly adapt to new environm

190 Influenza A viruses (IAVs) remain a significant public h

191 rough annual epidemics and global pandemics, influenza A viruses (IAVs) remain a significant threat t

192 h cell-tethered mucins modulate infection by influenza A viruses (IAVs) remain an open question.

193 Influenza A viruses (IAVs) represent repeatedly emerging

194 mphocyte (CTL) memory for pathogens like the influenza A viruses (IAVs), where the recall of IAV-spec

195 aintain a large, genetically diverse pool of influenza A viruses (IAVs), which can be transmitted to

196 Here, we tested the growth of influenza A virus in a subset of human cell lines and fo

197 Comparing SARS-CoV-2 and influenza A virus in human airway epithelial cultures, w

198 different hosts, we found that evolution of influenza A virus in mice did not necessarily proceed th

199 used by infection with Sendai virus (SeV) or influenza A virus in mice.

200 ant or escape such antibodies, we propagated influenza A virus in vitro with escalating concentration

201 en challenged by the identification of novel influenza A viruses in bats(1,2).

202 a model to study the growth and virulence of influenza A viruses in mammals but are not a natural hos

203 y MHC-II as a crucial entry mediator for bat influenza A viruses in multiple species, which permits a

204 eversion of 38T/F/M to I38-WT was rare among influenza A viruses in this study, suggesting stable ret

205 analyzed the virulence of pandemic H1N1 2009 influenza A viruses in vivo and in vitro.

206 vivo models of LPS-, Escherichia coli-, and influenza A virus-induced hyperinflammatory disease in a

207 n and inflammatory profiles between SeV- and influenza A virus-induced long-term lung disease.

208 tion of the Zalpha2 domain in ZBP1 abolished influenza A virus-induced PANoptosis and NLRP3 inflammas

209 demonstrate that this domain is critical for influenza A virus-induced PANoptosis and underlies perin

210 Nosocomial transmission of influenza A virus (InfA) infection is not fully recogniz

211 irus-specific CD8(+) T cells in the lungs of influenza A virus-infected mice.

212 Here, we examine the processes of influenza A virus infection and evolution in mice by com

213 ll (FNEC) culture model for investigation of influenza A virus infection and virus-host interactions.

214 In a disease context, influenza A virus infection impaired AM crawling via the

215 on of correlates of protection against human influenza A virus infection is important in development

216 ost dependency factors that are required for influenza A virus infection may serve as therapeutic tar

217 ow distinct functional characteristics after influenza A virus infection of B6 mice.

218 ined in hemizygous mice was also seen during influenza A virus infection, in which epitope-specific C

219 causes an impaired CD8(+) T cell response to influenza A virus infection, reduces T cell activation,

220 Using a mouse model of influenza A virus infection, we demonstrate that althoug

221 on in a respiratory dysbiosis model after an influenza A virus infection, when added therapeutically.

222 his response can be beneficial for the host: influenza A virus infection-induced pulmonary ectopic ge

223 ndomized, 223 were treated and had confirmed influenza A virus infection.

224 Hyperoxia at birth increases the severity of influenza A virus infections in adult mice by reducing t

225 at protect or predispose to severe and fatal influenza A virus infections is lagging.

226 The influenza A virus infects target cells through multivale

227 PORTANCE Successful zoonotic transmission of influenza A virus into humans can lead to pandemics in a

228 Influenza A virus is a pathogen of great medical impact.

229 tibody-induced selective pressure.IMPORTANCE Influenza A virus is a public health threat for which cu

230 The matrix-2 (M2) protein from influenza A virus is a tetrameric, integral transmembran

231 e the HA yield of vaccine viruses.IMPORTANCE Influenza A virus is a widespread pathogen that affects

232 The host range of an influenza A virus is determined by species-specific inte

233 Influenza A virus is highly contagious, infecting 5-15%

234 The genome of influenza A virus is organized into eight ribonucleoprot

235 genome into virions.IMPORTANCE The genome of influenza A virus is organized into eight viral ribonucl

236 f nuclear import of vRNP proteins.IMPORTANCE Influenza A virus is the major cause of influenza, a res

237 re we use a single-cell approach to quantify influenza A virus IVGs and examine their fitness implica

238 Two novel influenza A virus-like genomes were detected in fruit ba

239 The influenza A virus M1 and M2 proteins play important role

240 The amino terminus of influenza A virus matrix 2 ectodomain (M2e) is highly co

241 The influenza A virus matrix protein 2 ectodomain (M2e) is a

242 Influenza A virus matrix protein M1 is involved in multi

243 ce using coinfection with 1 x 10(4.5) PFU of influenza A virus MEM H3N2, followed by intranasal chall

244 cation in cells, prevented death in a lethal influenza A virus mouse challenge model, and dramaticall

245 A critical role of influenza A virus nonstructural protein 1 (NS1) is to an

246 The influenza A virus nucleoprotein (NP) is an essential mul

247 is Review, we examine the host barriers that influenza A viruses of animals, especially birds, must o

248 Zoonotic influenza A viruses of avian origin can cause severe dis

249 Seasonal influenza A viruses of humans evolve rapidly due to stro

250 lar rates of genetic change.IMPORTANCE While influenza A viruses of subtype H2N2 were at the origin o

251 The genomes of influenza A viruses of the H17N10 and H18N11 subtypes ha

252 or ovalbumin-induced airway inflammation and influenza A virus or Citrobacter rodentium infection alo

253 Influenza A virus PA-X is a fusion protein encoded in pa

254 a blueprint, we chose a mechanism typical of influenza A virus particles in which ectoenzymatic hemag

255 oded ANP32A proteins are required to support influenza A virus polymerase activity, and species diffe

256 The avian-origin influenza A virus polymerase is restricted in human cell

257 interactions between ANP32A proteins and the influenza A virus polymerase using split luciferase comp

258 igate its global propensity to interact with influenza A virus polymerase.

259 es across mammals appears critical to detect influenza A viruses posing a major threat to humans and

260 and HMPV preferred low temperatures; RSV and influenza A virus preferred a narrow "humidity-range" an

261 ry structure and microarray mapping, inhibit influenza A virus proliferation in MDCK cells.

262 ries probing the functions of this essential influenza A virus protein.

263 haemagglutinin, does not bind the canonical influenza A virus receptor, sialic acid or any other gly

264 on to identify antiviral genes that restrict influenza A virus replication.

265 l number of factors required for restricting influenza A virus replication.

266 Notably, the infection of mice with bat influenza A virus resulted in robust virus replication i

267 The evolution of influenza A viruses results in birth cohorts that have d

268 ransmission and mammalian adaptation of this influenza A virus, revealing changes in the hemagglutini

269 Intriguingly, although wild-type influenza A virus robustly triggers this SUMO switch in

270 d by many broadly neutralizing antibodies to influenza A virus, Sangesland et al. show that the V(H)1

271 , including that infection with a particular influenza A virus should offer long-term or lifelong pro

272 Opposite to that observed for influenza A virus sialidases and hNEU2, compounds with a

273 n papillomavirus-positive tumors, as well as influenza A virus-specific CD8(+) T cells in the lungs o

274 d using surface-immobilized HA and NA of the influenza A virus strain A/California/04/2009 and a nove

275 s in risk of influenza-associated disease by influenza A virus subtype can be seen in US influenza su

276 quent infections with antigenically distinct influenza A virus subtypes.

277 ene-regulatory networks are functional in an influenza A virus superinfection murine model of pneumon

278 Neutralizing antibodies targeting influenza A virus surface glycoproteins are critical com

279 We conducted influenza A virus surveillance among four bat species in

280 Our antibodies significantly protect highly influenza A virus susceptible BALB/c mice from lethal ch

281 Swine influenza A viruses (swIAVs) can play a crucial role in

282 r binding stability to the H3 protein of the influenza A virus than to the monovalent SA receptor.

283 urvival signals to CD4 T cells responding to influenza A virus that improve their memory fitness, ind

284 Moreover, influenza A viruses that are transmissible via the air p

285 Consistent with studies of influenza A viruses, the within-host evolution of IBVs i

286 inhibited by other RNA viruses, such as such influenza A virus, this innate immune signaling pathway

287 Susceptibility of influenza A viruses to baloxavir can be affected by chan

288 rise from the transmission of novel zoonotic influenza A viruses to humans(1,2).

289 ich anatomical site of the respiratory tract influenza A virus transmission occurs.

290 with previous reports, our data propose that influenza A virus uses a redundant and plastic network o

291 Thus, influenza A virus uses dual importin-betas for distinct

292 rived polyclonal Abs to the hemagglutinin of influenza A virus vaccine components, even with changes

293 this knowledge to design broadly protective influenza A virus vaccines.

294 r, of donors is a driver for transmission of influenza A viruses via the air.

295 Influenza A viruses were associated with an increased ri

296 Adults >=20 yo infected with influenza A viruses were more likely to show NA-only ser

297 rendered cells resistant to infection by bat influenza A virus, whereas ectopic expression of the HLA

298 -20 remain conserved across most subtypes of influenza A viruses, which explains the Ab's extraordina

299 enome packaging mechanism of an H7N7 subtype influenza A virus widely tolerates the mutation of indiv

300 However, treating mice infected with influenza A virus with this IL-2C reduces lung immunopat