ライフサイエンスコーパス: influenza A

1 nts have been reported to all treatments for influenza A.

2 ersally protective memory immune response to influenza A.

3 a target for a vaccine or treatment against influenza A.

4 ntly by viruses, primarily morbillivirus and influenza A.

5 salt bridge with an EC(50) = 2.7 muM against influenza A (A/WSN/1933).

6 We isolated influenza (A/Aichi/68; H3N2) virus:endosome conjugates f

7 15 and 2018, a total of 335 index cases with influenza A and 1,506 of their household contacts were e

8 HA of most influenza A and B (IAV/IBV) viruses is cleaved at a mono

9 in children (P = .29) and adults (P = .62), influenza A and B (P = .32), and other respiratory virus

10 evaluate the CD4(+) and CD8(+) responses to influenza A and B infection in a cohort of SOT patients.

11 oxil (BXM) was approved in 2018 for treating influenza A and B virus infections.

12 th exceptional breadth to multiple different influenza A and B virus neuraminidases.

13 had variable effects on in vitro fitness of influenza A and B viruses, but the ability of these viru

14 s fitness, replication, and pathogenesis for influenza A and B viruses.

15 fections from representative strains of both influenza A and B viruses.

16 reactivity with other virus antigens such as influenza A and HCoV, indicating high selectivity of the

17 outpatient setting, there were 1,666 and 274 influenza A and influenza B positives, respectively, acr

18 to 2019 influenza season and 1,857 and 1,449 influenza A and influenza B positives, respectively, dur

19 y in driving the asynchronous circulation of influenza A and rhinovirus.

20 The ID Now influenza A & B 2 (ID Now) assay (Abbott Laboratories),

21 Sofia influenza A+B FIA allows for surveillance of real-time d

22 Here, we demonstrate the novel use of Sofia influenza A+B fluorescent immunoassay (FIA), a rapid ant

23 luded COVID-19 (n=15: 12 active, 3 cleared), influenza A/B (n=6), and nonvirally mediated deaths (n=6

24 ne urgent care location using the Cobas LIAT Influenza A/B assay (LIAT assay; Roche Diagnostics, Indi

25 (ID Now) assay (Abbott Laboratories), Cobas influenza A/B nucleic acid test (LIAT; Roche Molecular S

26 easonal variation in the age distribution of influenza A cases suggests that factors other than age s

27 ility of 5a-5g to bind to the active site of influenza A CEN (PDB code: 6FS6) like baloxavir acid, 3.

28 One pediatric case, with picornavirus and influenza A coinfection, visited 3 different schools whi

29 ones to common viral epitopes (CMV, EBV, and influenza A) demonstrated that Ag specificity in VUE was

30 respiratory viruses, including an assay for influenza A (FluA) virus, influenza B (FluB) virus, and

31 Influenza A group 1 HA stem-nanoparticles have been demo

32 with low micromolar to nanomolar affinity to influenza A group 1 HAs.

33 human metapneumovirus A and B, influenza A, influenza A H1, influenza A H3, influenza A H1N1/2009, i

34 predictions for six contributing pathogens (influenza A/H1, A/H3, B, respiratory syncytial virus, an

35 during coinfection with an influenza virus, influenza A H1N1 A/Puerto Rico/8/1934 (PR8).

36 influenza A, influenza A H1, influenza A H3, influenza A H1N1/2009, influenza B, parainfluenza virus

37 challenge studies used the identical lot of influenza A (H1N1)pdm09 virus administered intranasally.

38 ratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfect

39 This is the case for human-origin influenza A(H1N1) pandemic 2009 (pdm09) viruses detected

40 cluding 22 oseltamivir-treated patients with influenza A(H1N1)pdm09 acute respiratory distress syndro

41 challenged intranasally using the identical influenza A(H1N1)pdm09 virus approximately 1 year apart.

42 identified the first case of a swine-origin influenza A(H1N1)pdm09 virus resulting in a human infect

43 vaccine products provide protection against influenza A(H1N1)pdm09, A(H3N2), and B lineage viruses.

44 VE against influenza A(H1N1)pdm09, A(H3N2), and B viruses were simi

45 from circulating human-associated strains of influenza A(H1N1)pdm09, and these signatures can be used

46 During the 2015-2016 US influenza A(H1N1)pdm09-predominant season, we found that

47 he HD than SD vaccine after stimulation with influenza A/H1N1 (1193 vs 0 per 106 CD4+ T cells; P = .0

48 superior than vaccine-elicited responses for influenza A/H1N1 (931 vs 1; p = 0.026), A/H3N2 (647 vs 1

49 Here we report the isolation of the influenza A/H1N1 2009 pandemic (A/H1N1pdm) and A/H3N2 vi

50 VE against deaths following confirmation of influenza A/H1N1 and A/H3N2, and against deaths with COP

51 re, pairs of genetically tagged and untagged influenza A/H1N1, A/H3N2 and A/H5N1 viruses that are tra

52 ional CD4+ and CD8+ T-cell responses against influenza A/H1N1, A/H3N2, and B.

53 s infected with a nearly identical strain of influenza A H1N1pdm09 (43 HCWs, 17 inpatients, and 6 wit

54 nged due to the emergence and circulation of influenza A/H1N1pdm09.

55 ovirus A and B, influenza A, influenza A H1, influenza A H3, influenza A H1N1/2009, influenza B, para

56 oligotypes on susceptibility differ between influenza A(H3N2) and B viruses.

57 k, to have similar transmission potential to influenza A(H3N2) in the same population.

58 % (95% CrI, 0.5-42%) lower susceptibility to influenza A(H3N2) infection, respectively.

59 (95% CI: 0.5%, 42%) lower susceptibility to influenza A(H3N2) infection, respectively.

60 We recruited 115 index cases with influenza A(H3N2) or B infection and 436 household conta

61 in both age groups, and wanes faster against influenza A(H3N2) than A(H1N1)pdm09.

62 The influenza A(H3N2) vaccine was updated from clade 3C.3a i

63 a season in the United States was high, with influenza A(H3N2) viruses predominating.

64 d Manufacturing Practices-produced wild-type influenza A(H3N2)2011 virus intranasally and were isolat

65 to 1436 cells per 10(6) CD4(+) T-cells among influenza A/H3N2 and B-infected patients (p = 0.006 and

66 Influenza A/H3N2 is a rapidly evolving virus which exper

67 n times and underlying antibody responses to influenza A/H3N2 using cross-sectional serum antibody re

68 henotypes.IMPORTANCE Highly pathogenic avian influenza A(H5N1) viruses have circulated continuously i

69 tions with clade 2.1 highly pathogenic avian influenza A/H5N1 virus have been reported, associated wi

70 s of polymerase activity, the higher 2016-17 influenza A(H5N8) virus virulence may be attributed to t

71 Highly pathogenic avian influenza A(H5N8) viruses first emerged in China in 2010

72 by characterizing the polymerase complex of influenza A(H5N8) viruses from both outbreaks.

73 indings suggest that the higher virulence of influenza A(H5N8) viruses from the 2016-17 outbreak may

74 he 2014-15 outbreak, the 2016-17 outbreak of influenza A(H5N8) viruses in the Netherlands and Europe

75 za virus virulence, and the gene segments of influenza A(H5N8) viruses reassorted extensively between

76 Influenza A(H5N8) viruses were first detected in the Net

77 In 2016, influenza A(H5N8) viruses were reintroduced into the Net

78 ation of primary duck cells with recombinant influenza A(H5N8) viruses, including viruses with reasso

79 luenza CVVs.IMPORTANCE The circulating avian influenza A(H7N9) has caused recurrent epidemic waves wi

80 Low-pathogenicity avian influenza A(H9N2) viruses, enzootic in poultry populatio

81 the relatively conserved stalk region of the influenza A hemagglutinin (HA) surface protein.

82 (M2e-MAbs) show protective potential against influenza A, however, they are either strain specific or

83 of human papilloma, vaccinia, dengue, Ebola, influenza A, human immunodeficiency, and hepatitis B vir

84 Influenza A (IAV) and influenza B (IBV) viruses are high

85 These data demonstrate a mechanism by which influenza A-induced STAT1 signaling inhibits neutrophil

86 uman PBMC culture, and increased survival of influenza A-infected mice.

87 on met criteria for a health care-associated influenza A infection (HCAI).

88 Hospitalized patients with influenza A infection were randomized 2:1 to receive pim

89 Our result, supported by data from influenza A infection, suggests that positive selection

90 m a previous household transmission study of influenza A infection, we confirm the result that the ma

91 navirus OC43, human metapneumovirus A and B, influenza A, influenza A H1, influenza A H3, influenza A

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

93 acle is producing a vaccine or treatment for influenza A is their universality or efficacy against no

94 Unlike influenza A M2 (AM2), which conducts protons with strong

95 T) to asparagine at residue 31 (S31N) in the influenza A M2 channel renders it insensitive to amantad

96 esponding to the transmembrane domain of the influenza A M2 protein (M2-TM).

97 The influenza A M2 protein is an acid-activated proton chann

98 ent resistance to inhibitors that target the influenza A M2 proton channel has necessitated a continu

99 The arrangement of histidine side chains in influenza A M2 tetramer determines their pK(a) values, w

100 influenza virus hemagglutinin and disrupted influenza A-mediated agglutination of human erythrocytes

101 lucidate the critical role of isotype for an influenza A monoclonal antibody therapeutic.

102 iruses detected by routine clinical testing (influenza A [n = 3], human metapneumovirus [n = 2], and

103 Participants with influenza A or B and without risk factors for complicati

104 on viral shedding in children infected with influenza A or B virus.

105 In a mouse model of severe influenza A pneumonia, we found the proinflammatory cyto

106 l loads were determined using a quantitative influenza A polymerase chain reaction (PCR).

107 Mice challenged with influenza A PR/8/34 H1N1 and subsequently challenged wit

108 tion using our recently described bireporter influenza A/Puerto Rico/8/34 (PR8) H1N1 (BIRFLU).

109 In contrast to Influenza A, PVM is substantially less lethal in IL-6 (-

110 Influenza A/Quebec/144147/2009 (H1N1)pdm09 and A/Switzer

111 vaccine and multiple therapeutic treatments, Influenza A remains a significant threat to human health

112 ANCE Influenza A virus is the major cause of influenza, a respiratory disease in humans and animals.

113 ore frequent in those <20 years old (yo) for influenza A (serosurvey, P = 0.01; immunology, P = 0.02)

114 utic agent, as it is highly conserved across influenza A serotypes, has a low mutation rate, and is e

115 3 further enables comprehensive subtyping of influenza A strains and multiplexed identification of do

116 antigenic drift and shift, resulting in new influenza A strains to which humans are naive.

117 ter activity profiles against drug-resistant influenza A strains, as well as influenza B, and improve

118 When H3N2 replaced H1N1 as the dominant influenza A subtype during the 2018-2019 season, the pat

119 nses to influenza and protection against new influenza A subtypes (phenomena known as original antige

120 Currently, two influenza A subtypes, A(H1N1) and A(H3N2), and type B vi

121 Targeting hemagglutinin from influenza A to Clec9A induced Ab responses with higher a

122 ed that the transmission bottleneck size for influenza A transmission between human hosts is small.

123 While influenza A transmission involves a tight population bot

124 M2e-MAbs show strong potential as universal influenza A treatments.IMPORTANCE Despite a seasonal vac

125 Pimodivir is a first-in-class antiviral for influenza A under development for these patients.

126 In the absence of a universal influenza A vaccine or treatment, influenza A will remai

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

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

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

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

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

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

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

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

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

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

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

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

139 Influenza A virus (IAV) causes significant morbidity and

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

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

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

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

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

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

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

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

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

149 Influenza A virus (IAV) infection during pregnancy cause

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 Influenza A virus (IAV) utilizes multiple strategies to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 Influenza A virus causes millions of severe cases of dis

190 The influenza A virus deploys this strategy to bind strongly

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

192 7-labeled full length M2 (M2FL) protein from Influenza A virus embedded in synthetic liquid crystalli

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 quent infections with antigenically distinct influenza A virus subtypes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 iral genome transcription and replication in influenza A virus.

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

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

248 disease following respiratory challenge with influenza A virus.

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

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

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

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

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

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

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

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

257 Influenza A viruses (IAV) sporadically transmit from swi

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

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

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

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

262 976 of waterfowl as the primary reservoir of influenza A viruses (IAVs) has since spurred decades of

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

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

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

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

267 Influenza A viruses (IAVs) represent repeatedly emerging

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

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

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

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

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

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

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

275 Influenza A viruses cause pandemics when they cross betw

276 Influenza A viruses cause widespread human respiratory d

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

278 Influenza A viruses continue to circulate among wild bir

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

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

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

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

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

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

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

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

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

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

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

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

291 smissibility, and interspecies adaptation of influenza A viruses.

292 was phylogenetically distinct from all other influenza A viruses.

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

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

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

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

297 the primary outcome, the OR in patients with influenza A was 0.94 (0.55-1.59) and was 3.19 (1.21-8.42

298 se 2b study, adults with acute uncomplicated influenza A were randomized 1:1:1:1 to receive one of th

299 universal influenza A vaccine or treatment, influenza A will remain a significant threat to human he

300 52 previously-healthy adult volunteers with influenza A/Wisconsin/67/2005 (H3N2) by intranasal inocu