ライフサイエンスコーパス: H7N9 virus

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

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

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

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

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

6 n asymptomatic or mild human infections with H7N9 viruses.

7 ning replication potential of newly emerging H7N9 viruses.

8 ation, pathogenicity and transmissibility of H7N9 viruses.

9 2013, which led to the zoonotic emergence of H7N9 viruses.

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

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

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

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

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

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

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

17 2013 was divergent from previously sequenced H7N9 viruses and more closely related to local circulati

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

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

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

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

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

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

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

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

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

27 H7N9 viruses are comparable to currently circulating inf

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 severe pulmonary disease observed following H7N9 virus infection.

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

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

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

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

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

111 The H7N9 virus isolated from the clinical patient in Guangdo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 All H7N9 viruses replicated efficiently in human bronchial e

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

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

131 Both H7N9 viruses replicated to higher titre in human airway

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 The H7N9 viruses were readily transmitted to naive ferrets t

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

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

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

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

172 013 was divergent from previously identified H7N9 viruses, with the NS and NP genes originating from

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