ライフサイエンスコーパス: H1N1 influenza virus

1 ed into recombinant A/Puerto Rico/8/34 (PR8) H1N1 influenza virus.

2 than did pigs infected with wild-type human H1N1 influenza virus.

3 terpene with remarkable activity against the H1N1 influenza virus.

4 ram) anti-influenza antibodies binding to an H1N1 influenza virus.

5 ere introduced into the genome of a seasonal H1N1 influenza virus.

6 e from a lethal challenge with 2009 pandemic H1N1 influenza virus.

7 ses and protective efficacy against pandemic H1N1 influenza virus.

8 he first reported cases of the pandemic 2009/H1N1 influenza virus.

9 cing infection with high viral loads of 2009 H1N1 influenza virus.

10 iruses and to specifically identify the 2009 H1N1 influenza virus.

11 oss-protection against the swine-origin 2009 H1N1 influenza virus.

12 otect against the pandemic swine-origin 2009 H1N1 influenza virus.

13 nt recipients; 4 were confirmed to have 2009 H1N1 influenza virus.

14 hospitalized transplant recipients with 2009 H1N1 influenza virus.

15 ss2, in knockout mice inhibits the spread of H1N1 influenza viruses.

16 nt as therapeutic agents against circulating H1N1 influenza viruses.

17 infection with two pandemic and two seasonal H1N1 influenza viruses.

18 tion H274Y in the neuraminidase (NA) gene of H1N1 influenza viruses.

19 ough the host was never exposed to the novel H1N1 influenza viruses.

20 urred in the HA of naturally occurring human H1N1 influenza viruses.

21 e from lethal challenges with either H5N1 or H1N1 influenza viruses.

22 resulted in a decrease in the replication of H1N1 influenza viruses.

23 cted with either 1918 or 2009 human pandemic H1N1 influenza viruses.

24 by a virus very similar to present swine (A/H1N1) influenza viruses.

25 o confer protection against a lethal dose of H1N1 influenza virus A/Puerto Rico 8/34 (PR8).

26 04 (VN1203), and the NA of the mouse-adapted H1N1 influenza virus A/Puerto Rico/8/34 (PR8) in the VSV

27 of cell death is a distinguishing feature of H1N1 influenza virus A/Puerto Rico/8/34 protein PB1-F2.

28 s were protected from challenge with a novel H1N1 influenza virus (A/California/07/2009), and these f

29 r M-Tri-DAP and subsequently challenged with H1N1 influenza virus (A/England/195/2009).

30 vector encoding the hemagglutinin (HA) of an H1N1 influenza virus (A/Swine/Indiana/1726/88) to porcin

31 structure in complex with HA from a pandemic H1N1 influenza virus, A/South Carolina/1/1918(H1N1), rev

32 eplaced with genes from a contemporary human H1N1 influenza virus, A/Texas/36/91 (Tx/91), were genera

33 nversion, ferrets were challenged with novel H1N1 influenza virus and assessed for viral titers in th

34 ted to understand better the pathogenesis of H1N1 influenza virus and associated host mucosal immune

35 with escalating concerns regarding the novel H1N1 influenza virus and its recently approved vaccine,

36 mechanism underlying broad immunity against H1N1 influenza viruses and identifies a conserved epitop

37 , Muc5ac-Tg animals were challenged with PR8/H1N1 influenza viruses and showed significant decreases

38 Exposure to multiple seasonal H1N1 influenza viruses, and not to any single H1N1 influ

39 natural history and transmission of the 2009 H1N1 influenza virus appear to be similar to those of pr

40 In early 2009, a novel pandemic H1N1 influenza virus appeared, but it has not exhibited

41 ferrets with antigenically distinct seasonal H1N1 influenza viruses boosts the antibody responses dir

42 However, oseltamivir-resistant H1N1 influenza viruses carrying the H275Y NA mutation sp

43 Oseltamivir-resistant H1N1 influenza viruses carrying the H275Y neuraminidase

44 ast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, repl

45 ity and improved protection against the 2009 H1N1 influenza virus, compared with subcutaneous injecti

46 e, the X-181 strain of the 2009 new pandemic H1N1 influenza virus, derived from the A/California/07/2

47 e hemagglutinin and nucleoprotein genes from H1N1 influenza virus developed serum anti-H1 immunoglobu

48 nstrate that memory CD4 T cells specific for H1N1 influenza virus directed protective responses to in

49 reover, sequential infection of ferrets with H1N1 influenza viruses elicited an Igkappa-biased Ab res

50 expressing NA from avian (H5N1) or pandemic (H1N1) influenza virus, elicited NA-specific antibody and

51 1N1 influenza viruses, and not to any single H1N1 influenza virus, elicits a breadth of antibodies th

52 A novel H1N1 influenza virus emerged in 2009 (pH1N1) to become t

53 In 2009, a novel H1N1 influenza virus emerged in humans, causing a global

54 The rapid dissemination of the 2009 pandemic H1N1 influenza virus emphasizes the need for universal i

55 is report, we show that recombinant H5N1 and H1N1 influenza viruses encoding a truncated NS1 protein

56 evidence supporting the hypothesis that the H1N1 influenza virus entered the human population just p

57 The 2009 A(H1N1) influenza viruses exhibited less efficient respira

58 Primary infection with s-H1N1 influenza virus followed by a dose of p-LAIV result

59 een preferentially eliminated from classical H1N1 influenza virus genomes during virus evolution in h

60 , the avian-derived PB2 of the 2009 pandemic H1N1 influenza virus has 271A.

61 The emergence of the pandemic 2009 H1N1 influenza virus has become a world-wide health conc

62 Swine origin 2009 H1N1 influenza virus has spread globally to cause the fi

63 Drug-resistant H1N1 influenza viruses have dominated the 2009 flu seaso

64 Thus, our data show that 2009 H1N1 influenza viruses have evolved after pandemic onset

65 re is increasing evidence that 2009 pandemic H1N1 influenza viruses have evolved after pandemic onset

66 g the emergence and global spread of a novel H1N1 influenza virus in 2009, two A(H1N1)pdm/09 influenz

67 en associated with the 2009-2010 pandemic of H1N1 influenza virus in China and with mass vaccination

68 The transmissibility of the 2009 H1N1 influenza virus in households is lower than that se

69 ve relevance to pathogenesis of the pandemic H1N1 influenza virus in humans; thus, pigs may serve as

70 ne from an H5N1 virus rescued replication of H1N1 influenza virus in macrophages.

71 h displayed an EC50 value of 2.1 muM against H1N1 influenza virus in MDCK cells.

72 We show that infection with H1N1 influenza virus in mice that lack B and T cells (Re

73 The spread of the 2009 H1N1 influenza virus in the population worldwide, in add

74 We show that pandemic H1N1 influenza virus in which the hemagglutinin signal s

75 essential for the spread and pathogenesis of H1N1 influenza viruses in mice.

76 mmalian (swine H1N1, human H1N1 and pandemic H1N1) influenza viruses in PAM.

77 hile the seroprevalence of seasonal H3N2 and H1N1 influenza viruses increased with the decline of amb

78 The estimated rate of admission for pandemic H1N1 influenza virus infection in pregnant women during

79 dation to promptly treat pregnant women with H1N1 influenza virus infection with anti-influenza drugs

80 nstrated lung regeneration in mice following H1N1 influenza virus infection, and linked distal airway

81 lated form as new therapeutic agents against H1N1 influenza virus infection.

82 protects ferrets against aerosol-transmitted H1N1 influenza virus infection.

83 revention of disease and control of pandemic H1N1 influenza virus infection.

84 ) to mediate protection against swine-origin H1N1 influenza virus infection.

85 A remarkable feature of the 2009 pandemic H1N1 influenza virus is its efficient transmissibility i

86 ily accelerated clearance of a 2009 pandemic H1N1 influenza virus isolate in an antibody-dependent ma

87 based vaccine for both seasonal and pandemic H1N1 influenza virus isolates.

88 The 2009 H1N1 influenza virus outbreak is the first pandemic of t

89 The 1918 H1N1 influenza virus pandemic was the most severe of the

90 omestic pigs infected with the 2009 pandemic H1N1 influenza virus (pH1N1) have been detected worldwid

91 death from infection with the 2009 pandemic H1N1 influenza virus (pH1N1).

92 ss-species transmission of the 2009 pandemic H1N1 influenza virus (pH1N1).

93 Subsequent human infections with novel H1N1 influenza viruses prompted an investigation of the

94 damage and high lethality caused by the 1918 H1N1 influenza virus remains largely unknown.

95 regulated in the lungs of patients with 2009 H1N1 influenza virus, respiratory syncytial virus, or pa

96 major concern about the ongoing swine-origin H1N1 influenza virus (S-OIV) outbreak is that the virus

97 luenza A and B viruses, including a pandemic H1N1 influenza virus strain, a highly pathogenic H5N1 av

98 ed to the disappearance of existing seasonal H1N1 influenza virus strains.

99 Pigs infected with recombinant human H1N1 influenza virus that carried the H5N1 NS gene exper

100 we determined the ability of representative H1N1 influenza viruses that circulated in the human popu

101 h seasonal H1N1 and triple-reassortant swine H1N1 influenza viruses that have circulated among North

102 For H1N1 influenza viruses, the mouse-adapted A/WSN/33 strai

103 humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better unde

104 The 2009 H1N1 influenza virus was first identified in April 2009

105 ted with highly pathogenic H5N1 and seasonal H1N1 influenza viruses was evaluated using mass spectrom

106 Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by char

107 H1N1 influenza viruses were responsible for the 1918 pan

108 ortment between H3N2 human and classic swine H1N1 influenza viruses, while the others arose from reas

109 t and infectious HIV, hepatitis C virus, and H1N1 influenza virus, whole-genome gene expression analy

110 in ferrets infected with any single seasonal H1N1 influenza viruses, with limited protection to chall

111 oled and tested for the presence of the 2009 H1N1 influenza virus without a reduction in sensitivity.