ライフサイエンスコーパス: H7N9 virus

1 in 28 of them (1%); all tested negative for H7N9 virus.

2 minimise the risk of human infection with A H7N9 virus.

3 se traits were tested in the context of an A/H7N9 virus.

4 anges to the immunological properties of the H7N9 virus.

5 of human infection with an avian influenza A(H7N9) virus.

6 isease in China caused by avian influenza A (H7N9) virus.

7 n asymptomatic or mild human infections with H7N9 viruses.

8 ning replication potential of newly emerging H7N9 viruses.

9 ation, pathogenicity and transmissibility of H7N9 viruses.

10 iruses with genes derived from both H9N2 and H7N9 viruses.

11 ence of antigenically distinct LPAI and HPAI H7N9 viruses.

12 y to fuse at a lower pH threshold than other H7N9 viruses.

13 s HA from pandemic 1968 H3N2 and recent 2013 H7N9 viruses.

14 2013, which led to the zoonotic emergence of H7N9 viruses.

15 of mice infected with A(H5Nx), A(H6N1), or A(H7N9) viruses.

16 are essential for mammalian adaptation of A(H7N9) viruses.

17 essed the replication ability of three human H7N9 viruses (A/Anhui/1/2013, A/Shanghai/1/2013, A/Shang

18 ly, the NP of the newly emerged avian-origin H7N9 virus also contains an asparagine at position 52 an

19 ined the receptor-binding properties of this H7N9 virus and compared them with those of an avian H7N3

20 ize the characteristic features of the novel H7N9 viruses and assess their pandemic potential.

21 2013 was divergent from previously sequenced H7N9 viruses and more closely related to local circulati

22 A virus vaccination were able to neutralize H7N9 viruses and protect mice against homologous challen

23 magglutination-inhibiting antibodies against H7N9 viruses and protected mice from stringent viral cha

24 ity, and transmissibility of A/Anhui/1/2013 (H7N9) virus and variants in vitro and in vivo using a sy

25 ay have been critical for the emergence of A(H7N9) viruses and their ability to infect humans.

26 Inspections of protein sequences from A(H7N9) viruses and their immediate predecessors revealed

27 es at genetic level responding to the lethal H7N9 virus are still poorly understood.

28 H7N9 viruses are able to bind to human sialic acid recep

29 Sporadic infections by H5N1, H5N6, and H7N9 viruses are also reported.

30 Both H5N1 and H7N9 viruses are capable of causing lethal infections, w

31 H7N9 viruses are comparable to currently circulating inf

32 hese findings suggest that the current human H7N9 viruses are poorly adapted for efficient human-to-h

33 MERS-CoV and H7N9 viruses are still a major worldwide public health c

34 uman infections with influenza A(H5N1) and A(H7N9) viruses are now annual seasonal occurrences in Asi

35 s (NAIs) in humans infected with influenza A(H7N9) viruses are public health concerns.

36 to the emergence of the A/Guangdong/1/2013 (H7N9) virus as a novel H7N9 virus in Guangdong, China, a

37 s of avian [A(H5N1), A(H5N6), A(H7N7), and A(H7N9) viruses associated with severe human disease] or s

38 jiang to other provinces and the presence of H7N9 viruses at live poultry markets have fuelled the re

39 Our results show that the emerging H7N9 virus attached moderately or abundantly to both upp

40 Interestingly, A(H7N9) virus budded from the surfaces of both ciliated an

41 lutination-inhibiting antibodies against the H7N9 virus, but we unexpectedly found high titers of ADC

42 oped and were tested for the presence of the H7N9 virus by means of real-time RT-PCR.

43 ry changes at amino acid position 217 in the H7N9 viruses can serve as a genetic marker for virus ant

44 Therefore, while A(H7N9) virus can infect mammals, further adaptation appea

45 The hemagglutinin glycoprotein of most human H7N9 viruses carries Leu(226), a residue linked to adapt

46 thogenic avian H5N1 and the recently emerged H7N9 viruses cause severe infections in humans, often wi

47 mitted to humans, and some, such as H5N1 and H7N9 viruses, cause severe disease in humans.

48 18, the novel A/Anhui/1/2013 (AH/13)-lineage H7N9 virus caused at least five waves of outbreaks in hu

49 On 30 March 2013, a novel avian influenza A H7N9 virus causing severe human respiratory infections w

50 ng 24, 48, or 72 hours after A/Anhui/1/2013 (H7N9) virus challenge.

51 Furthermore, many of the H7N9 viruses circulating in animal reservoirs contain pu

52 immunized animals.IMPORTANCE Avian influenza H7N9 viruses circulating in poultry and wild birds conti

53 H9N2-derived PB2 and PA genes in H7N9 virus conferred enhanced polymerase activity in hum

54 g variation at the NA catalytic residue of A(H7N9) viruses, conferred reduced inhibition by laninamiv

55 The newly emerging H7N9 viruses constitute an obvious public health concern

56 Four NA variants of A/Taiwan/1/2013(H7N9) virus containing a single substitution (NA-E119V,

57 entering the fourth wave of human infection, H7N9 viruses continue to exhibit genetic diversity in av

58 Influenza H7N9 virus continues to cause infections in humans and r

59 ily clusters, human-to-human transmission of H7N9 virus could not be ruled out.

60 ons within the HA and PB2 genes of the novel H7N9 viruses created by reverse genetics in an important

61 In pulmonary endothelial cells, A(H7N9) virus efficiently initiated infection; however, no

62 In March 2013, a novel influenza A(H7N9) virus emerged in China as an unexpected cause of s

63 etic studies have indicated that the novel A(H7N9) viruses emerged from reassortment of H7, N9, and H

64 mportance: The genomes of the zoonotic avian H7N9 viruses emerging in China have mutations in critica

65 Human infections by avian influenza A(H7N9) virus entail substantial morbidity and mortality.

66 Here, we found that, just prior to the fifth H7N9 virus epidemic, H9N2 viruses had phylogenetically m

67 genotype that was responsible for the fifth H7N9 virus epidemic.

68 Collectively, our results suggest that IAV(H7N9) viruses evolve in chickens through antigenic drift

69 These results also shed light on how the H7N9 virus evolved, which is critically important for fu

70 es in pH fusion threshold identified between H7N9 viruses examined.

71 of Tc caprine with inactivated influenza A (H7N9) viruses followed by H7N9 Hemagglutinin 1 (HA1) boo

72 tant H1N1 and heterosubtypic H3N2, H5N1, and H7N9 viruses for at least 6 months while maintaining lun

73 prior to intranasal infection with H5N1 and H7N9 viruses for prophylaxis, and 24, 48, and 72 hours p

74 tic acid to asparagine at position 701) of A(H7N9) viruses for mammalian adaptation.

75 sequence of two chicken source influenza A (H7N9) viruses found in Guangdong live poultry market (LP

76 s (SIAs) compared to a closely related avian H7N9 virus from 2008.

77 Similar to first-wave viruses, H7N9 viruses from 2013 to 2015 were highly infectious in

78 y, CR8020 escape mutation is seen in certain H7N9 viruses from recent outbreaks.

79 Genetically, some H7N9 viruses from the fifth wave have acquired novel ami

80 and PA genes in the generation of a dominant H7N9 virus genotype (G72) with enhanced infectivity in h

81 lating H7N9 virus to create a novel dominant H7N9 virus genotype that was responsible for the fifth H

82 hanges confer drug resistance of influenza A(H7N9) viruses (group 2NA) remains sparse.

83 Since 2013, avian H7N9 virus had caused five sequential human epidemics in

84 A(H7N9) viruses had the highest relative risk at the time

85 The avian influenza A H7N9 virus has caused infections in human beings in Chin

86 e results suggest that the highly pathogenic H7N9 virus has pandemic potential and should be closely

87 cle, these results suggest that the emerging H7N9 virus has the potential both to transmit efficientl

88 rotein and virus that the NA of the zoonotic H7N9 viruses has a binding capacity via both the seconda

89 The emergence of avian H7N9 viruses has raised concerns about its pandemic pote

90 blic health, as the avian-origin influenza A(H7N9) virus has caused more than 1,560 laboratory-confir

91 l antibodies against antigenically drifted A(H7N9) viruses has not been evaluated before.

92 c avian H5N1 virus and, more recently, avian H7N9 virus have resulted in high rates of lethality in h

93 Our results also suggest that H7N9 viruses have become enzootic in China and may sprea

94 hreat for poultry.IMPORTANCE Avian influenza H7N9 viruses have been causing disease outbreaks in poul

95 Recently, HPAI H7N9 viruses have evolved into different subtypes and ge

96 AI H7N9 viruses suggests that the fifth-wave H7N9 viruses have evolved to acquire novel traits with t

97 gether, we conclude that the fifth-wave HPAI H7N9 viruses have gained the ability to cause enhanced d

98 ution since their initial detection in 2013, H7N9 viruses have maintained a pathogenic phenotype in m

99 Although the fifth-wave H7N9 viruses have not yet gained the ability to transmit

100 Here we show that H7N9 viruses have spread from eastern to southern China

101 Our results indicate that H7N9 viruses have the capacity for efficient replication

102 Two epidemic waves of an avian influenza A (H7N9) virus have so far affected China.

103 Influenza A(H7N9) viruses have caused a large number of zoonotic inf

104 Human infections caused by avian influenza A(H7N9) viruses have raised concerns of a pandemic.

105 ) virus (A[H1N1]pdm09) and avian influenza A(H7N9) virus hemagglutinins (HAs) despite being seronegat

106 H15, and H7 (derived from the novel Chinese H7N9 virus) hemagglutinins.

107 e of H9N2 virus in the continual mutation of H7N9 virus highlights the public health significance of

108 wing a pathway similar to that of the recent H7N9 virus, highlights the role of domestic ducks and th

109 es-were in clusters different from those for H7N9 viruses identified previously in other provinces of

110 have contributed to the spread of the novel H7N9 viruses.IMPORTANCE Novel H7N9 IAVs continue to caus

111 than 300 human infections with a novel avian H7N9 virus in China indicates that this emerging strain

112 The emergence of the H7N9 virus in China is another reminder of the threat of

113 e A/Guangdong/1/2013 (H7N9) virus as a novel H7N9 virus in Guangdong, China, and that viral adaptatio

114 tudy, we conducted enhanced surveillance for H7N9 virus in Guangdong, China, from April to August 201

115 ated and characterized the avian influenza A H7N9 virus in Guangdong, China, from April to August 201

116 chieve this, we propagated low-pathogenicity H7N9 virus in the presence of polyclonal antiserum deriv

117 We previously determined that propagation of H7N9 virus in virus-specific antiserum gives rise to mut

118 sette determines the transmission fitness of H7N9 viruses in chickens, and the reassortment events ca

119 structures of NAs from human-infecting avian H7N9 viruses in complex with five human anti-N9 antibodi

120 ight some distinctive properties of H5N1 and H7N9 viruses in different in vitro and in vivo models.

121 The emergence of avian H7N9 viruses in humans in China has renewed concerns abo

122 es with high neutralizing activities against H7N9 viruses in vitro.

123 infection, the pathogenic mechanism of the A(H7N9) virus in humans is largely unknown.

124 ere similarities between particular H5N1 and H7N9 viruses, including association between lethal disea

125 o acid changes on the evolutionary path to A(H7N9) viruses, including substitutions that may be assoc

126 Influenza A (H7N9) virus induced high mortality since 2013.

127 cies barrier, as in early 2013 when an avian H7N9 virus infected humans in China.

128 healthy infants, children and adults against H7N9 virus-infected cells and recombinant hemagglutinin

129 High titers of ADCC-Abs against H7N9 virus-infected cells were detected in sera from adu

130 elated strongly with ADCC-Abs titers against H7N9 virus-infected cells.

131 Most persons with confirmed H7N9 virus infection had severe lower respiratory tract

132 unt for the sharp increase in human cases of H7N9 virus infection in the 2016-2017 epidemic.

133 ut all laboratory-confirmed human cases of A H7N9 virus infection reported in mainland China as of Fe

134 The median age of patients with H7N9 virus infection was older than other patient groups

135 Every identified human case of A H7N9 virus infection was required to be reported to Chin

136 Among 139 persons with confirmed H7N9 virus infection, the median age was 61 years (range

137 To provide insights into the pathogenesis of H7N9 virus infection, we compared risk factors, clinical

138 provide complete protection against group 2 H7N9 virus infection, while the variant loses protection

139 d H7 protein failed to protect chickens from H7N9 virus infection.

140 ns were conducted for each confirmed case of H7N9 virus infection.

141 linical evaluation to protect humans from wt H7N9 virus infection.

142 virus enabling role during highly pathogenic H7N9 virus infection.

143 IFI35 deficiency protected mice from H7N9 virus infection.

144 severe pulmonary disease observed following H7N9 virus infection.

145 first identified cases of avian influenza A(H7N9) virus infection in humans occurred in China during

146 ver time, with identification of influenza A(H7N9) virus infections in humans, as well as detection o

147 Human infection with avian influenza A(H7N9) virus is associated mainly with the exposure to in

148 Sequence analyses showed that the Guangdong H7N9 virus isolated from April to May shared high sequen

149 The H7N9 virus isolated from the clinical patient in Guangdo

150 e relative virulence and transmissibility of H7N9 viruses isolated during the second and third waves,

151 To determine if H7N9 viruses isolated from humans during 2013 to 2015 ha

152 e ability of first-, second-, and third-wave H7N9 viruses isolated from humans to cause disease in mi

153 The A/Guangdong/1/2013 (H7N9) virus isolated from the Guangdong patient on 10 Au

154 Influenza A(H7N9) viruses isolated from humans show features suggest

155 ity of A/Anhui/1/2013 and A/Shanghai/1/2013 (H7N9) viruses, isolated from fatal human cases, to cause

156 w-pathogenic avian influenza (LPAI) and HPAI H7N9 virus isolates from the fifth epidemic wave were as

157 that a single mutation, L217Q, in the HA of H7N9 virus led to 23- and 8-fold reductions in hemagglut

158 Thus, the hemagglutinin of the A/H7N9 virus may adopt traits associated with airborne tra

159 n immunity to the emergent avian influenza A(H7N9) virus, neuraminidase inhibitors are vital for cont

160 Sporadic human infections by a novel H7N9 virus occurred over a large geographic region in Ch

161 vel highly pathogenic avian influenza (HPAI) H7N9 viruses of the fifth epidemic wave infect humans an

162 ng ensuing transmission events, the Anhui/13 H7N9 virus outcompeted 2:6 H7N9 AIVs with internal gene

163 However, the H7N9 viruses overcome this restriction by harboring an N

164 ruses with pandemic potential, such as avian H7N9 virus, particularly against those carrying drug res

165 al distribution and genetic diversity of the H7N9 viruses poses a direct challenge to current disease

166 In contrast, HPAI H7N9 viruses possessed enhanced virulence, causing great

167 of human illnesses due to avian influenza A(H7N9) virus provided reason for US public health officia

168 n host; and (iii) both wild-type and variant H7N9 viruses rapidly develop additional mammalian-signat

169 It is unclear how the H7N9 virus re-emerged and how it will develop further; p

170 itutions in transmission and pathogenesis of H7N9 viruses remain unclear.

171 All H7N9 viruses replicated efficiently in human bronchial e

172 The highly pathogenic H7N9 viruses replicated efficiently in mice, ferrets, an

173 Several high- and low-pathogenicity H7N3 and H7N9 viruses replicated efficiently in the respiratory t

174 Both H7N9 viruses replicated to higher titre in human airway

175 In epithelial cells, A(H7N9) virus replicated efficiently but did not elicit ro

176 Furthermore, A(H7N9) virus replicated to a significantly higher titer a

177 esistant seasonal influenza A(H3N2) viruses, H7N9 virus replication and pathogenicity in these models

178 The mutant H7N9 viruses representing escape mutations containing an

179 While the A(H7N9) virus resulted in a significant epidemic in China

180 d deep sequencing analysis revealed that the H7N9 viruses sampled after transmission showed a reduced

181 Conversely, H7N9 viruses showed a greater tropism for respiratory ep

182 Moreover, the H7N9 viruses showed greater infectivity and lethality in

183 Sporadic human infections with H7N9 viruses started being reported in China in the earl

184 ensure that current research with first-wave H7N9 viruses still pertains to more recently isolated st

185 study investigated the N9 NA from a zoonotic H7N9 virus strain in order to determine its possible rol

186 The A(H7N9) virus strain that emerged in 2013 was associated w

187 H5N1 virus subtype, or the avian influenza A H7N9 virus subtype.

188 ty to fuse at a lower pH threshold than LPAI H7N9 viruses suggests that the fifth-wave H7N9 viruses h

189 , through reassortment, for the emergence of H7N9 viruses that cause severe human infections.

190 tibodies against the antigenically drifted A(H7N9) viruses that emerged recently during the fifth-wav

191 ors revealed several amino acid changes in A(H7N9) viruses that may have facilitated transmission and

192 ion to genome segments derived from an avian H7N9 virus, the H7N3 virus reassorted efficiently with t

193 After the isolation of the first A(H7N9) viruses, the nucleotide sequences became publicall

194 ur internal genes of the A/Guangdong/1/2013 (H7N9) virus-the NS, NP, PB1, and PB2 genes-were in clust

195 protects mice against lethal challenge with H7N9 virus through mechanisms likely involving antibody-

196 nces between the low- and high-pathogenicity H7N9 viruses, thus playing a major role in their antigen

197 Ferrets were then challenged with wild-type H7N9 virus to assess the vaccine's protective efficacy.

198 tations, were reassorted into co-circulating H7N9 virus to create a novel dominant H7N9 virus genotyp

199 inding assays, and ferret studies reveal the H7N9 virus to have increased binding to mammalian respir

200 n NP results in increased sensitivity of the H7N9 virus to human Mx, indicating that this residue is

201 itical mutations (i.e., HA-Q226L) enable the H7N9 viruses to be transmitted in a mammalian host and s

202 The ability of HPAI H7N9 viruses to cause more severe disease and to replica

203 Since then, multiple transmissions of H7N9 viruses to humans have occurred, leaving experts pu

204 Improved adaptation of A(H7N9) virus to human upper airway poses an important thr

205 In this study, we assessed the ability of A(H7N9) virus to infect, replicate, and elicit innate immu

206 volutionary analysis of the progenitors of A(H7N9) viruses to identify amino acid changes that may ha

207 to assess the susceptibility of influenza A(H7N9) viruses to oseltamivir, the most prescribed anti-i

208 The recent human infections with H7N9 virus, totalling over 130 cases with 39 fatalities

209 owever, limited, nonsustained human-to-human H7N9 virus transmission could not be ruled out in four f

210 Mx-mediated inhibition and might explain why H7N9 viruses transmitted efficiently to humans.

211 have a confirmed case if the presence of the H7N9 virus was verified by means of real-time reverse-tr

212 ntial pandemic risk posed by avian influenza H7N9 viruses was heightened during the fifth epidemic wa

213 Among group 2 HA viruses tested, a single A(H7N9) virus was not neutralized at 50 mug/ml; it contain

214 6+2" reassortant H9N9 (having NP and NA from H7N9) virus was shed from contact chickens in a signific

215 To trace the source of the avian H7N9 viruses, we collected 99 samples from 4 live poultr

216 be linked to the antigenic change among the H7N9 viruses, we serially passaged the viruses in the pr

217 ay also have contributed to the genesis of A(H7N9) viruses, we inferred historical evolutionary event

218 laboratory-confirmed human infections with A H7N9 virus were reported in mainland China, with 134 cas

219 All of the fifth-wave H7N9 viruses were able to transmit among cohoused ferret

220 H7N3 and H7N9 viruses were also detected in the mouse eye followi

221 H5N1, H7N7, and H7N9 viruses were pathogenic in mice, and this pathogeni

222 The H7N9 viruses were readily transmitted to naive ferrets t

223 Human infections with the avian influenza A(H7N9) virus were first reported in China in 2013 and con

224 ntly emerged A(H5N2), A(H5N8), A(H6N1), or A(H7N9) viruses were protected from mortality and showed d

225 We compared a low pathogenic H7N9 virus with a highly pathogenic isolate, and two of

226 in mice and ferrets than the low pathogenic H7N9 virus, with the exception of the neuraminidase inhi

227 013 was divergent from previously identified H7N9 viruses, with the NS and NP genes originating from

228 Quantitative screening of influenza A (H7N9) virus without DNA amplification was performed base