ライフサイエンスコーパス: influenza A virus infection

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

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

3 an important factor in the pathogenicity of influenza A virus infection.

4 in mediastinal lymph nodes and HSI to lethal influenza A virus infection.

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

6 ntribute to pulmonary inflammation following influenza A virus infection.

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

8 mponents and TLR3 as crucial for immunity to influenza A virus infection.

9 ecognition by the immune system during human influenza A virus infection.

10 tter understand correlates of protection for influenza A virus infection.

11 toxicity and Th1 CD4 T-cell development upon influenza A virus infection.

12 t, in turn, alert T cells to the presence of influenza A virus infection.

13 ossible roles of anti-M2 antibodies in human influenza A virus infection.

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

15 se, thus providing better protection against influenza A virus infection.

16 innate immune cells was highly protective in influenza A virus infection.

17 ls and some bird species (such as duck) upon influenza A virus infection.

18 ific T cells isolated directly ex vivo after influenza A virus infection.

19 he tested bat cell lines were susceptible to influenza A virus infection.

20 it increased susceptibility and mortality to influenza A virus infection.

21 unreported antiviral function of MxA against influenza A virus infection.

22 (in chronic Hepatitis C virus patients) and Influenza A virus infection.

23 e, we compare these effectors directly after influenza A virus infection.

24 l, to treat suspected or confirmed 2009 H1N1 influenza A virus infection.

25 lay an important role in the pathogenesis of influenza A virus infection.

26 virus that should not cross-protect against influenza A virus infection.

27 binant viruses protected mice against lethal influenza A virus infection.

28 tion and, thus, increased protection against influenza A virus infection.

29 ct. when expressed in its natural context of influenza A virus infection.

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

31 have implications for approaches to control influenza A virus infection.

32 ugs used for the prevention and treatment of influenza A virus infections.

33 such does not fully protect mice from lethal influenza A virus infections.

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

35 nza-associated pneumonia similar to seasonal influenza A virus infection and accounts for a substanti

36 school-aged children, compared with seasonal influenza A virus infection and noninfluenza ILI.

37 compared participants with rRT-PCR-confirmed influenza A virus infection and test-negative controls.

38 fection were compared to those with seasonal influenza A virus infection and those with ILI who had n

39 of 132 RSV infections were compared with 144 influenza A virus infections and with all non-RSV infect

40 helial expression of Ear1 functions to limit influenza A virus infection, and its loss contributes to

41 y used worldwide for the treatment of severe influenza A virus infection, and should drug-resistant p

42 Known therapies for influenza A virus infection are complicated by the frequ

43 ts that anti-M2 antibody responses following influenza A virus infection are weak and/or transient.

44 Furthermore, we demonstrate that herpes and influenza A virus infections are enhanced when host circ

45 ding EPS15 at endosomes, thereby influencing influenza A virus infection as well as degradation of EG

46 s, whereas cytospin-enhanced DFA detected 31 influenza A virus infections as well as 3 respiratory sy

47 ay an important role in host defense against influenza A virus infection, but we have now discovered

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

49 demonstrate that p53 isoforms play a role in influenza A virus infection by using silencing and trans

50 and MCP-1 in HMEE cells activated by a prior influenza A virus infection compared to levels in cells

51 DCs or blocking CD28 after day 6 of primary influenza A virus infection decreases the virus-specific

52 Under these experimental conditions, influenza A virus infection did not produce detectable a

53 We showed that influenza A virus infection does not generate dsRNA and

54 ing that LGP2, a host protein induced during influenza A virus infection, downregulates the host anti

55 e to the increased morbidity associated with influenza A virus infection during pregnancy.

56 09 vaccine for preventing medically attended influenza A virus infection during the 2010-2011 season.

57 tigen testing in the laboratory diagnosis of influenza A virus infection during the current 2009 H1N1

58 reptococcus pneumoniae while recovering from influenza A virus infection exhibit exacerbated disease

59 estigate antiviral and cytokine responses to influenza A virus infection, focusing on the contributio

60 transparent and a cohort with an antecedent influenza A virus infection, followed by i.n. inoculatio

61 Adamantanes have been used to treat influenza A virus infections for many years.

62 ntified that best discriminate patients with influenza A virus infection from patients with either E

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

64 s and plasmacytoid dendritic cells (pDCs) to influenza A virus infection in 21 pregnant and 21 nonpre

65 the role of skeletal muscle during systemic influenza A virus infection in any host and particularly

66 mmatory hormone that reduces the severity of influenza A virus infection in females.

67 esults suggest that the cellular response to influenza A virus infection in human lung cells is signi

68 Bak is substantially downregulated during influenza A virus infection in MDCK cells, and the knock

69 , similarly to our previous observation that influenza A virus infection in the presence of a pancasp

70 to summarize the role of innate immunity in influenza A virus infection in the young child and to hi

71 Murine Ifitm3 controls influenza A virus infection in vivo, and polymorphisms i

72 Influenza A virus infections in humans generally cause s

73 as been shown to confer strong resistance to influenza A virus infections in mice.

74 Vesicular stomatitis virus and influenza A virus infection increased IFITM3-K88me1 leve

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

76 Influenza A virus infection induces massive inflammation

77 Influenza A virus infection is a major source of morbidi

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

79 Influenza A virus infection is mediated via binding of t

80 IFN receptor, we demonstrate that intranasal influenza A virus infection leads to the robust type III

81 mune-competent children and that a preceding influenza A virus infection may not provide cross-protec

82 ll, our data show that the repeated low-dose influenza A virus infection mouse model is more stringen

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

84 We describe the characterization of influenza A virus infection of an established in vitro m

85 ed type I IFN production triggered by RSV or influenza A virus infection of BALB/c mice and found tha

86 Influenza A virus infection of C57BL/6 mice is a well-ch

87 66 and acid polymerase PA224 epitopes during influenza A virus infection of C57BL/6 mice.

88 Influenza A virus infection of mice deficient for IFN-ga

89 e production and cytokine sensitivity during influenza A virus infection of primary tracheal epitheli

90 This investigation assessed the effects of influenza A virus infection on both the patency and resp

91 eam effects of NS1 protein expression during influenza A virus infection on global cellular mRNA leve

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

93 and inflammation, we examined the effects of influenza A virus infection on tolerance induced by expo

94 During H1N1 influenza A virus infection, platelets display activatio

95 l-aged, compared with patients with seasonal influenza A virus infection (prevalence ratio [PR], 2.0;

96 ion to critical illness associated with 2009 influenza A virus infection remains uncertain.

97 We show that influenza A virus infection results in increased product

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

99 Subsequent to influenza A virus infection, there was a significant dif

100 ame strain in combination with an antecedent influenza A virus infection to colonize the nasopharynx

101 the A2G mouse strain are highly resistant to influenza A virus infections, to both mono- and polybasi

102 The effectiveness of TIV against influenza A virus infection was 63% (95% confidence inte

103 Of 2002 admissions, influenza A virus infection was diagnosed in 3.5% (71),

104 The response of plasmacytoid DCs to influenza A virus infection was not impaired.

105 nitude of H-2(k)-restricted CTL responses to influenza A virus infection was similar in the F(1) hybr

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

107 Using a mouse model of influenza A virus infection, we found that CD8 effector

108 e role of this dsRNA-binding activity during influenza A virus infection, we generated a recombinant

109 viral and cellular protein synthesis during influenza A virus infection, we used recombinant influen

110 The influenza EIA detected 16 influenza A virus infections, whereas cytospin-enhanced

111 ndance of the tested miRNAs to the extent of influenza A virus infection, which initiates primary miR

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

113 s identified cellular genes triggered during influenza A virus infection whose expression was strictl

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