ライフサイエンスコーパス: influenza A

1 tudies presented pediatric-specific data; 35 influenza A and 16 influenza B studies presented adult-s

2 Forty-six influenza A and 24 influenza B studies presented pediatr

3 d the negative predictive value for both the influenza A and B assay was 81%.

4 NAATs had markedly higher sensitivities for influenza A and B in both children and adults than did t

5 then operated test devices on site to detect influenza A and B in those specimens.

6 The effect is observed for both influenza A and B strains in groups of subjects vaccinat

7 s correctly able to detect, type and subtype influenza A and B virus strains directly from clinical s

8 ategy was validated on thousands of seasonal influenza A and B virus-positive specimens using multipl

9 Influenza A and B viruses and respiratory syncytial viru

10 Influenza A and B viruses are one of the most common cau

11 Influenza A and B viruses are the causative agents of an

12 The influenza A and B viruses are the primary cause of seaso

13 raminidase [NA], and matrix [M]) of seasonal influenza A and B viruses for next-generation sequencing

14 cines is to provide broad protection against influenza A and B viruses.

15 diverse natural histories, including Ebola, influenza A, and severe acute respiratory syndrome (SARS

16 ructure and functions of the M2 protein from Influenza A are sensitive to pH, cholesterol, and the an

17 ximately 70% accurate using in-house qRT-PCR influenza A as a gold-standard comparison.

18 a is an acute respiratory illness, caused by influenza A, B, and C viruses, that occurs in local outb

19 We developed a single-reaction influenza A/B virus (FluA/B) multiplex reverse transcrip

20 y 12.1 to 31.8 percentage points, except for influenza A by rapid NAATs (2.7 percentage points).

21 In this report, we used a novel Influenza A/California/04/09 (H1N1) reporter virus that

22 er, in response to in vitro stimulation with influenza A/California/7/2009 (H1N1) Ag, differential ge

23 es (CIVs) are the causative agents of canine influenza, a contagious respiratory disease in dogs, and

24 Device performance for influenza A detection was approximately 70% accurate usi

25 Pooled sensitivities for detecting influenza A from Bayesian bivariate random-effects model

26 anomolar affinity and neutralization against influenza A group 1 viruses, including the 2009 H1N1 pan

27 A) and neuraminidase (NA) genes of this seal influenza A(H10N7) virus revealed that it was most close

28 it was most closely related to various avian influenza A(H10N7) viruses.

29 Influenza A H15 viruses are members of a subgroup (H7-H1

30 Here, we show that both 2009 pandemic H1N1 influenza A (H1N1) virus and highly pathogenic avian inf

31 The 2009 pandemic influenza A(H1N1) (A[H1N1]pdm09) vaccine component has r

32 After 2009, pandemic influenza A(H1N1) [A(H1N1)pdm09] cocirculated with A(H3N

33 interval [CI], 2.61-6.13) for 2009 pandemic influenza A(H1N1) and 1.76 (95% CI, 1.33-2.32) for influ

34 adults >/=65 y were significantly higher for influenza A(H1N1) and A(H1N1)pdm09 compared to A(H3N2) a

35 pandemic A(H1N1) vaccine have supported that influenza A(H1N1) vaccination does not increase the risk

36 To evaluate whether pandemic influenza A(H1N1) vaccination in pregnancy increases the

37 cies, offspring exposed and unexposed to the influenza A(H1N1) vaccine during pregnancy were matched

38 se results support the safety profile of the influenza A(H1N1) vaccine used in pregnancy.

39 was characterized by a delayed 2009 pandemic influenza A(H1N1) virus (A[H1N1]pdm09) epidemic and conc

40 ccine (LAIV) or who had laboratory-confirmed influenza A(H1N1) virus infection.

41 ine (ISV) targeting monovalent 2009 pandemic influenza A(H1N1) virus or live-attenuated influenza vac

42 Infections with influenza A(H1N1) was suggested to be more serious than

43 Among patients with 2009 pandemic influenza A(H1N1), ratios for hIVIG (n = 9) versus place

44 arly as 14 days after vaccination but not to influenza A(H1N1).

45 vaccination for influenza A(H3N2) (p=0.004), influenza A(H1N1)pdm09 (p=0.01), and influenza B viruses

46 Analyses included 596 influenza A(H1N1)pdm09 and 305 B(Victoria) cases and 926

47 reater than zero for at least six months for influenza A(H1N1)pdm09 and influenza B and at least five

48 fectiveness of current and prior inactivated influenza A(H1N1)pdm09 vaccination from influenza season

49 ent inactivated AS03-adjuvanted split virion influenza A(H1N1)pdm09 vaccine (Pandemrix; GlaxoSmithKli

50 ) and influenza B and 6% - 11% per month for influenza A(H1N1)pdm09 viruses.

51 We included 3376 patients with influenza A(H1N1)pdm09, of whom 3085 (91.4%) had laborat

52 ared to individuals never vaccinated against influenza A(H1N1)pdm09, the highest effectiveness (66%;

53 per-protocol population (53.8% vs 37.6% for influenza A(H1N1)pdm; 48.1% vs 32.3% for influenza A(H3N

54 Biotinylated influenza A/H1N1 and A/H5N1 as well as adenovirus seroty

55 Similar results were observed for influenza A/H1N1, influenza A/H3N2, and influenza B stra

56 outcomes among critically ill patients with influenza A (H1N1pdm09) in Mexican and Canadian hospital

57 Four patients with influenza A/H1N1pdm09 in the oseltamivir group developed

58 Influenza A H3N2 variant [A(H3N2)v] viruses have caused

59 Influenza A H3N2 variant [A(H3N2)v] viruses, which have

60 E with increasing time since vaccination for influenza A(H3N2) (p=0.004), influenza A(H1N1)pdm09 (p=0

61 reactivity among humans primed with seasonal influenza A(H3N2) (sH3N2), using postinfection ferret an

62 ts had >/=4-fold antibody titer rise against influenza A(H3N2) and B antigens following vaccination;

63 e in VE of about 7% (absolute) per month for influenza A(H3N2) and influenza B and 6% - 11% per month

64 vels of serum antibodies and salivary IgA to influenza A(H3N2) and influenza B virus strains as early

65 nza A(H1N1) and 1.76 (95% CI, 1.33-2.32) for influenza A(H3N2) and influenza B.

66 nst medically attended, laboratory-confirmed influenza A(H3N2) illness was estimated by test-negative

67 Influenza A(H3N2) infection was laboratory-confirmed in

68 Recent outbreaks of swine-origin influenza A(H3N2) variant (H3N2v) viruses have raised pu

69 features related to low pathogenicity avian influenza A(H3N2) viruses and were distinct from A(H3N8)

70 The rapid evolution of influenza A(H3N2) viruses necessitates close monitoring

71 and influenza B and at least five months for influenza A(H3N2) viruses.

72 Influenza A(H3N2) was identified in 166 (12%) individual

73 for influenza A(H1N1)pdm; 48.1% vs 32.3% for influenza A(H3N2); and 90.7% vs 75% for influenza B; P <

74 A total of 181 cases of influenza A/H3N2, 47 cases of influenza B, and 6 cases o

75 results were observed for influenza A/H1N1, influenza A/H3N2, and influenza B strains.

76 es of representative highly pathogenic avian influenza A(H5) viruses from Vietnam were generated, com

77 enged with lethal doses of highly pathogenic influenza A H5N1 or H1N1 viruses.

78 uman infections with highly pathogenic avian influenza A (H5N1) virus are frequently fatal but the me

79 a A (H1N1) virus and highly pathogenic avian influenza A (H5N1) virus induce expression of tumor necr

80 ion is increasing, and human infections with influenza A(H5N1) and A(H7N9) viruses are now annual sea

81 the emergence of human infections with avian influenza A(H5N1) and has evolved over time, with identi

82 unogenicity and protective efficacy of avian influenza A(H5N1) vaccine.

83 ted 2 human cases of highly pathogenic avian influenza A(H5N1) virus infection, detected through popu

84 and reassortment of highly pathogenic avian influenza A(H5N1) viruses at the animal-human interface

85 7; 10.3%) were significantly more at risk of influenza A(H7N1) infection (P = .001) than those in oth

86 e first case of cat-to-human transmission of influenza A(H7N2), an avian-lineage influenza A virus, t

87 The avian influenza A H7N9 virus has caused infections in human be

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

89 Quantitative screening of influenza A (H7N9) virus without DNA amplification was p

90 e full-length sequence of two chicken source influenza A (H7N9) viruses found in Guangdong live poult

91 as evolved over time, with identification of influenza A(H7N9) virus infections in humans, as well as

92 molecular changes confer drug resistance of influenza A(H7N9) viruses (group 2NA) remains sparse.

93 Influenza A(H7N9) viruses have caused a large number of

94 ign high-avidity trimeric proteins that bind influenza A hemagglutinin (HA) at its conserved receptor

95 , we analyzed NS1 protein variability within influenza A (IAV) H3N2 viruses infecting humans during t

96 Using simulations and case studies (influenza A in lesser snow geese and Yersinia pestis in

97 After influenza A infection of immunologically naive ferrets w

98 ecular diagnostic assay for the detection of influenza A, influenza B, and RSV.

99 ed the pathogenicity and transmissibility of influenza A/Italy/3/2013 virus in mouse and ferret model

100 cluding activity against Ebola virus and bat influenza A-like virus, and we describe here their phylo

101 ses circulating in bats, including Ebola and influenza A-like viruses.

102 Although influenza A M2 (AM2) and B M2 (BM2) are functional analo

103 tanes are well-established inhibitors of the influenza A M2 proton channel, the mechanisms by which t

104 fluenza A/Panama/2007/99 (H3N2) and pandemic influenza A/Netherlands/602/2009 (H1N1) viruses.

105 shown to lower the limit of detection of an influenza A nucleoprotein immunoassay by over 50%.

106 dults (including pregnant women) with severe influenza A or B (defined as the presence of hypoxia or

107 criptase polymerase chain reaction-confirmed influenza A or B virus in all participants (vaccinated c

108 on IAV reassortment using the human seasonal influenza A/Panama/2007/99 (H3N2) and pandemic influenza

109 We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic process

110 D-Ad-vaccinated animals after challenge with influenza A/PR/8/34 virus.

111 to express the hemagglutinin (HA) gene from influenza A/PR/8/34 virus.

112 esponses were subsequently investigated upon influenza A/Puerto Rico/8/34 infection using a Western d

113 itor significantly reduced the activation of influenza A/Scotland/20/74 virions, providing further ev

114 formulations including the hemagglutinins of influenza A subtypes H1N1 and H3N2 and B lineages Yamaga

115 ed on the IAV hemagglutinin, seven different influenza A viral groups (VGs) were identified.

116 ion and its downstream effects responding to influenza A virus (A/WSN/33 [H1N1]), tumor necrosis fact

117 Influenza A virus (IAV) and influenza B virus (IBV) caus

118 When hemagglutinin (HA) glycoproteins from influenza A virus (IAV) are expressed in cells, ER stres

119 Influenza A virus (IAV) causes an acute infection in hum

120 Influenza A virus (IAV) causes up to half a million deat

121 y CD4 T cell recall following heterosubtypic influenza A virus (IAV) challenge of mice primed previou

122 The genome of influenza A virus (IAV) comprises eight RNA segments (vR

123 Influenza A virus (IAV) consists of eight viral RNA (vRN

124 Influenza A virus (IAV) continues to pose an enormous an

125 Influenza A virus (IAV) expresses m(6)A-modified RNAs, b

126 Influenza A virus (IAV) genomes are composed of eight si

127 The emergence of the novel influenza A virus (IAV) H7N9 since 2013 has caused conce

128 We have shown that glycosylation of influenza A virus (IAV) hemagglutinin (HA), especially a

129 Using a murine model of influenza A virus (IAV) infection and a panel of chromos

130 allergic inflammation was protective against influenza A virus (IAV) infection and disease.

131 Exaggerated inflammatory responses during influenza A virus (IAV) infection are typically associat

132 he outcome of infectious diseases, including influenza A virus (IAV) infection, are rarely evaluated.

133 respiratory epithelial cells in response to influenza A virus (IAV) infection, as well as the CHIP-s

134 es in our understanding of the mechanisms of influenza A virus (IAV) infection, the crucial virus-hos

135 empers the intensity of the host response to influenza A virus (IAV) infection.

136 We then apply our method to a data set of influenza A virus (IAV) infections for which viral deep-

137 The pathogenesis of influenza A virus (IAV) infections is a multifactorial p

138 Influenza A virus (IAV) is an RNA virus that is cytotoxi

139 s of infections, but its role in immunity to influenza A virus (IAV) is not well studied.

140 ing it with the well-characterized viroporin influenza A virus (IAV) matrix-2 protein.

141 Influenza A virus (IAV) nonstructural protein 1 (NS1) is

142 S and human and mouse genetics, we show that influenza A virus (IAV) ribogenesis and growth are suppr

143 Influenza A virus (IAV) RNA packaging signals serve to d

144 e T cells in children to genetically diverse influenza A virus (IAV) strains to which the children ha

145 rcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were investigated in vitro and i

146 Two subtypes of influenza A virus (IAV), avian-origin canine influenza v

147 SV-1), encephalomyocarditis virus (EMCV) and influenza A virus (IAV), we identified several TRIM prot

148 to humans have enhanced the virulence of the influenza A virus (IAV).

149 d virus Epstein-Barr virus (EBV), as well as influenza A virus (IAV).

150 g infection, including RNA and proteins from influenza A virus (IAV).

151 ding protein 1 (ZBP1) as an innate sensor of influenza A virus (IAV).

152 ed mortality after infectious challenge with influenza A virus (IAV).

153 then coinfected them with mouse-adapted H1N1 influenza A virus (PR/8/34).

154 Specifically, we inoculated 2D2 mice with influenza A virus (Puerto Rico/8/34; PR8) and then monit

155 on the virion surface, is important in both influenza A virus assembly and entry.

156 been previously identified to play a role in influenza A virus assembly were found to complement the

157 The NS1 protein from all strains of influenza A virus binds TRIM25, although not all virus s

158 The data suggest that influenza A virus budding and genome incorporation can o

159 Influenza A virus causes pandemics and annual epidemics

160 able of conferring protection in a stringent influenza A virus challenge.

161 discuss the implications of reassortment for influenza A virus evolution, including its classically r

162 A major factor that determines influenza A virus fitness and therefore transmissibility

163 acid receptors.IMPORTANCE The interaction of influenza A virus glycoproteins with cell surface recept

164 H15 is the other member of the subgroup of influenza A virus group 2 hemagglutinins (HAs) that also

165 n.Broadly reactive antibodies that recognize influenza A virus HA can be protective, but the mechanis

166 ffinity relationship for interactions of the Influenza A virus HA with bivalent displays of the natur

167 al replication, the M2 proton channel of the influenza A virus has been the focus of many studies.

168 Influenza A virus hemagglutinin (HA) initiates viral ent

169 chy to the five major antigenic sites in the influenza A virus hemagglutinin globular domain.

170 The emergence of avian H7N9 influenza A virus in humans with associated high mortali

171 ceptives, levonorgestrel, impacts sequential influenza A virus infection by modulating antibody respo

172 Although it is well established that Influenza A virus infection is initiated in the respirat

173 Susceptibility to colitis and influenza A virus infection occurring upon commensal bac

174 describe the imprinting by the initial first influenza A virus infection on the antibody response to

175 ed influenza, we identified 13 children with influenza A virus infection who were subsequently infect

176 sponses are important for protection against influenza A virus infection, that these can be most effi

177 uate the microminipig as an animal model for influenza A virus infection, we compared the receptor di

178 ficantly affect adaptive immune responses to influenza A virus infection, with their effect on the ou

179 ed to an elevated cellular susceptibility to influenza A virus infection.

180 the microminipig as a novel animal model for influenza A virus infection.

181 ipig could serve as a novel model animal for influenza A virus infection.

182 S2 plays an important and unexpected role in influenza A virus infection.

183 es the ThCTL that develop in the lung during influenza A virus infection.

184 ominipigs represent a novel animal model for influenza A virus infection.

185 etween younger and aging mice in response to influenza A virus infection.IMPORTANCE Influenza virus i

186 Emerging evidence from vaccinia and influenza A virus infections indicates that subsets of c

187 fluenza B virus infections than for treating influenza A virus infections.

188 e identified 10 independent introductions of influenza A virus into Ohio and/or Indiana exhibition sw

189 y to promote their nuclear export.IMPORTANCE Influenza A virus is a major pathogen of a wide variety

190 Influenza A virus is a threat for humans due to seasonal

191 ergetic barrier to pore expansion.IMPORTANCE Influenza A virus is an airborne pathogen causing season

192 sm underlying the genetic diversification of influenza A virus is reassortment of intact gene segment

193 Similarly, challenge with influenza A virus led to increased infiltration of the v

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

195 identified a mutation at position 76 of the influenza A virus M2 protein that drastically reduces in

196 results suggest that PB1-F2 from H7N9 avian influenza A virus may be a major contributory factor to

197 Influenza A virus mRNAs are transcribed by the viral RNA

198 In contrast, the influenza A virus NS1 protein interacts with RIG-I and T

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

200 we identify several acetylation sites of the influenza A virus nucleoprotein (NP), including the lysi

201 Attachment of the Influenza A virus onto host cells involves multivalent i

202 reactive oxygen species production abrogates influenza A virus pathogenicity.

203 Avian influenza A virus polymerases typically do not function

204 VX-787 is an inhibitor of the influenza A virus pre-mRNA cap-binding protein PB2.

205 The Influenza A virus RdRp in contrast, uses a capped RNA ol

206 nsider the constraints and drivers acting on influenza A virus reassortment, including the likelihood

207 Exogenous SPL expression inhibited influenza A virus replication, which correlated with an

208 role for TRIM25 in specifically restricting influenza A virus replication.

209 all, this work advances our understanding of influenza A virus RNA synthesis and identifies the initi

210 virus, in 1958, 16 different novel, zoonotic influenza A virus subtype groups in 29 countries, Taiwan

211 le anilines were identified as inhibitors of influenza A virus subtype H1N1, and extensive chemical s

212 Two influenza A virus subtypes has been reported in dogs in

213 r cases of human infection by emerging avian influenza A virus subtypes, including H7N9 and H10N8 vir

214 Influenza A virus suppresses the translation of host mRN

215 Through active influenza A virus surveillance in US exhibition swine an

216 In this paper, the prospect of detecting influenza A virus using digital ELISA has been studied.

217 the Aries Flu A/B & RSV assay were 98.1% for influenza A virus, 98.0% for influenza B virus, and 97.7

218 n antiviral response, whereas infection with influenza A virus, herpes simplex virus 1, or cytomegalo

219 ssion of influenza A(H7N2), an avian-lineage influenza A virus, that occurred during an outbreak amon

220 Coinfection with influenza A virus, which also expresses a neuraminidase,

221 tion of specific peptides from vaccinia- and influenza A virus-encoded proteins.

222 ng CD4 effector population, and they mediate influenza A virus-specific cytotoxic activity.

223 confirmed by analyzing different strains of influenza A virus.

224 the wild-type and V27A mutant M2 channels of influenza A virus.

225 redundant bystander during coinfection with influenza A virus.

226 serve as the principal natural reservoir for influenza A virus; however, the key properties of NA for

227 Influenza A viruses (IAV) can cause lung injury and acut

228 ng to the genetic and antigenic diversity of influenza A viruses (IAV) currently circulating in swine

229 Avian influenza A viruses (IAV) of the H9N2 subtype have succe

230 ope tag in the C terminus of PB1 resulted in influenza A viruses (IAV) that are safe and effective as

231 interactomes between human host and several influenza A viruses (IAV).

232 ne are one of the main reservoir species for influenza A viruses (IAVs) and play a key role in the tr

233 uenza virus pathogenesis.IMPORTANCE Seasonal influenza A viruses (IAVs) are among the most common cau

234 ion of genetically and antigenically diverse influenza A viruses (IAVs) are circulating among the swi

235 Influenza A viruses (IAVs) are endemic in swine and repr

236 ve vaccine approaches against IAV.IMPORTANCE Influenza A viruses (IAVs) are one of the most common ca

237 key role in the ecology and transmission of influenza A viruses (IAVs) between species.

238 reassortment is segment dependent.IMPORTANCE Influenza A viruses (IAVs) can exchange genes through re

239 sonal influenza viruses in humans.IMPORTANCE Influenza A viruses (IAVs) cause acute infection of the

240 Influenza A viruses (IAVs) cause seasonal epidemics and

241 Influenza A viruses (IAVs) continue to threaten animal a

242 n variability in subjects infected with H3N2 influenza A viruses (IAVs) during the 2010/2011 season w

243 ortment of gene segments between coinfecting influenza A viruses (IAVs) facilitates viral diversifica

244 equenced the genomes of 441 wild-bird origin influenza A viruses (IAVs) from North America and subjec

245 are critical for activating HAs of seasonal influenza A viruses (IAVs) in humans.

246 ) that neutralizes both group I and group II influenza A viruses (IAVs) in vitro.

247 Different influenza A viruses (IAVs) infect the same cell in a hos

248 The risk of emerging pandemic influenza A viruses (IAVs) that approach the devastating

249 Reassortment among influenza A viruses allows viruses to expand their host

250 sisting of globular head domains from exotic influenza A viruses and stalk domains from influenza B v

251 is one of the major surface glycoproteins of influenza A viruses and the target for the influenza dru

252 ral activities against currently circulating influenza A viruses and their genetic barrier to drug re

253 of the influenza virus RNA genome.IMPORTANCE Influenza A viruses are a major global health threat, no

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

255 Influenza A viruses are constantly changing.

256 Human infections with novel influenza A viruses are of global public health concern,

257 Segment reassortment and base mutagenesis of influenza A viruses are the primary routes to the rapid

258 H7 subtype influenza A viruses are widely distributed and have been

259 Low-pathogenic (LP) avian H7 influenza A viruses are widely distributed in the avian

260 moprophylaxis of human infections with novel influenza A viruses associated with severe human illness

261 ons probably need to be acquired by emerging influenza A viruses before they can spread in the human

262 Influenza A viruses can also cause sporadic infections o

263 Zoonotic transmission of influenza A viruses can give rise to devastating pandemi

264 NPs from all strains of influenza A viruses contain two nuclear localization sig

265 Antibodies capable of neutralizing divergent influenza A viruses could form the basis of a universal

266 A panel of influenza A viruses expressing chimeric hemagglutinins (

267 Influenza A viruses generally mediate binding to cell su

268 Influenza A viruses have caused a number of global pande

269 the disease-causing potential of LP avian H7 influenza A viruses in mammals may be underestimated, an

270 to pigs resulted in substantial evolution of influenza A viruses infecting swine, contributing to the

271 influenza epidemics that can be severe, and influenza A viruses intermittently cause pandemics.

272 Reassortment of influenza A viruses is an important driver of virus evol

273 The RNA genome of influenza A viruses is transcribed and replicated by the

274 sible reassortment of human and other animal influenza A viruses presents an ongoing risk to public h

275 New influenza A viruses that emerge frequently elicit compos

276 ) is a sialidase expressed on the surface of influenza A viruses that releases progeny viruses from t

277 Influenza A viruses that successfully established stable

278 vessel for the generation of novel pandemic influenza A viruses through reassortment because of thei

279 ary for introduction and adaptation of avian influenza A viruses to mammalian hosts is important for

280 und that the sensitivity of microminipigs to influenza A viruses was the same as that of larger minia

281 pig, and the sensitivity of microminipigs to influenza A viruses was the same as that of miniature pi

282 Although vaccines confer protection against influenza A viruses, antiviral treatment becomes the fir

283 sistant to highly pathogenic avian H5 and H7 influenza A viruses, but were almost as susceptible to i

284 tiviral efficacy against multidrug-resistant influenza A viruses, in vitro drug resistance barrier, a

285 y against several human clinical isolates of influenza A viruses, including both oseltamivir-sensitiv

286 ne are actively involved in the evolution of influenza A viruses, including zoonotic strains.

287 ain, implicated in host range restriction of influenza A viruses, is still poorly understood.

288 ists in more than 95% of current circulating influenza A viruses, targeting the AM2-S31N proton chann

289 can wild birds are an important reservoir of influenza A viruses, yet the potential of viruses in thi

290 basic 2 (PB2) and the nucleoprotein (NP) of influenza A viruses.

291 r insights into the replication mechanism of influenza A viruses.

292 le in the defense of mammalian cells against influenza A viruses.

293 ted to affect the temperature sensitivity of influenza A viruses.

294 ard ducks, the natural host and reservoir of influenza A viruses.

295 assessment of the pandemic risk of zoonotic influenza A viruses.

296 virucidal for H1 hemagglutinin-bearing human influenza A viruses.

297 pacts multiple steps in viral replication of influenza A viruses.

298 which mouse MX1 interacts with the incoming influenza A vRNPs and inhibits their activity by disrupt

299 f influenza B, and 6 cases of nonsubtypeable influenza A were detected.

300 cts enveloped RNA and DNA viruses, including influenza A, Zika, Ebola, Sindbis, vesicular stomatitis,