ライフサイエンスコーパス: Ebola virus infection

1 several ISGs not previously known to affect Ebola virus infection.

2 There are no approved therapies for Ebola virus infection.

3 emographic variables and exposure level with Ebola virus infection.

4 tic efficacy in a non-human primate model of Ebola virus infection.

5 asures for post-exposure prophylaxis against Ebola virus infection.

6 and translate it into treatment options for Ebola virus infection.

7 ed intracellular cholesterol trafficking and Ebola virus infection.

8 an increase in the probability of surviving Ebola virus infection.

9 s what is known about the natural history of Ebola virus infection.

10 nterventions for controlling the outbreak of Ebola virus infection.

11 e the cellular immune responses during acute Ebola virus infection.

12 erspectives for treatment strategies against Ebola virus infection.

13 ll travellers at highest risk of exposure to Ebola virus infection.

14 ness and multiple organ failure secondary to Ebola virus infection.

15 further improved protective efficacy against Ebola virus infection.

16 es affect the efficacy of protection against Ebola virus infection.

17 tinct disease phenotypes after mouse-adapted Ebola virus infection.

18 important role in the immunopathogenesis of Ebola virus infection.

19 development of antiviral compounds to combat Ebola virus infection.

20 mediated immune responses in protection from Ebola virus infection.

21 n the clearance and protection against fatal Ebola virus infection.

22 t the innate immune system, for treatment of Ebola virus infection.

23 are potentially critical for survival after Ebola virus infection.

24 d a decisive role for NK cells during lethal Ebola virus infection.

25 critical to protection against subcutaneous Ebola virus infection.

26 ting that this receptor is not essential for Ebola virus infection.

27 promising candidate for immunoprophylaxis of Ebola virus infection.

28 y to the Ebola virus glycoprotein, enhancing Ebola virus infection.

29 ected upto 100% of naive mice against lethal Ebola virus infection.

30 polyclonal immune serum in a mouse model of Ebola virus infection.

31 and would play a role in the pathogenesis of Ebola virus infection.

32 d to cure animals from this otherwise lethal Ebola virus infection.

33 e design and as a prophylactic agent against Ebola virus infection.

34 utic agents for the treatment and control of Ebola virus infections.

35 ca experienced an unanticipated explosion of Ebola virus infections.

36 in 28 646 suspected, probable, and confirmed Ebola virus infections.

37 velopment of circulatory shock seen in fatal Ebola virus infections.

38 t immune responses during the acute phase of Ebola virus infection, a finding that would not have bee

39 Patients with Ebola virus infections admitted to university hospitals

40 e demonstration that CTLs can prevent lethal Ebola virus infection affects vaccine development in tha

41 Cellular cathepsins are required for Ebola virus infection and are believed to proteolyticall

42 Therefore, TPC proteins play a key role in Ebola virus infection and may be effective targets for a

43 e with VLPs had no protective effect against Ebola virus infection and NK cells treated with VLPs pro

44 T cells are required for natural immunity to Ebola virus infection and that CD4-dependent antibody re

45 tible models to BDBV infection as well as to Ebola virus infection and that no virus adaptation is re

46 ostic test is needed to confirm outbreaks of Ebola virus infection and to distinguish it from other d

47 ing vaccine candidate for protection against Ebola virus infections and a much needed tool to examine

48 verage human levels survived otherwise fatal Ebola virus infections and became immune to virus rechal

49 al growth, provide protection against lethal Ebola virus infection, and may not require participation

50 Ebola virus infections are characterised by immune suppr

51 tenuates lethality in experimental models of Ebola virus infection but - similar to findings in bacte

52 Ebola virus infection causes a highly lethal hemorrhagic

53 In human Ebola virus infection, clinical outcome is strongly asso

54 e chain reaction (RT-PCR)-based diagnosis of Ebola virus infection currently requires a blood sample

55 eful for the analysis of immune responses to Ebola virus infection, development of neutralizing antib

56 Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms

57 of GP was thought to be an essential step in Ebola virus infection, generation of a viable mutant Ebo

58 Existing models of Ebola virus infection have not fully characterized the p

59 virus GP(1,2), as well as Marburg virus and Ebola virus infection in a dose-dependent manner and at

60 recorded zoonotic transmission to humans and Ebola virus infection in bats and primates (1976-2014).

61 et of illness and laboratory confirmation of Ebola virus infection in Europe or the United States, an

62 Zaire Ebola virus infection in macaques causes a fatal disease

63 were effective for detecting and containing Ebola virus infection in newly imported nonhuman primate

64 in rAd5-GP-induced immune protection against Ebola virus infection in NHPs.

65 ribe a highly effective vaccine strategy for Ebola virus infection in non-human primates.

66 Vaccine-induced immunity to Ebola virus infection in nonhuman primates (NHPs) is mar

67 ible to develop a preventive vaccine against Ebola virus infection in primates.

68 43-year-old medical doctor who contracted an Ebola virus infection in Sierra Leone on Nov 16, 2014 (d

69 s or serological testing was used to confirm Ebola virus infection in suspected cases.

70 A record number of people survived Ebola virus infection in the 2013-16 outbreak in west Af

71 btain a diverse experimental data set of the Ebola virus infection in vitro, and then make use of Bay

72 , including those with proposed relevance to Ebola virus infection in vivo, such as endothelial cells

73 The current outbreak of Ebola virus infection in West Africa, with >26 000 cases

74 of death for both mother and fetus following Ebola virus infection is extremely high.

75 Ebola virus infection is highly lethal and leads to seve

76 Ebola virus infection is initiated by interactions betwe

77 ement of the joints in acute or convalescent Ebola virus infection is not well characterized in human

78 March 2015, the largest recorded outbreak of Ebola virus infection is ongoing, with almost 25 000 cas

79 The results support the concept that Ebola virus infection is self-contained in NHPs infected

80 The ability to rapidly recognize Ebola virus infections is critical to quickly limit furt

81 tissue damage in fatal EVD, and suggest that Ebola virus infection may induce aberrant neutrophils wh

82 Ebola virus infections mediated by mucosal exposure, and

83 dy-positive HHCs suggests that mild cases of Ebola virus infection occurred and that the full extent

84 Thus, Ebola virus infection of one target cell may induce biol

85 Consistent with these observations, Ebola virus infection of Vero cells activated neither tr

86 bola virus-positive woman was diagnosed with Ebola virus infection on her first day of life.

87 ment was accelerated in response to the 2014 Ebola virus infection outbreak.

88 or amplify proinflammatory signaling during Ebola virus infection, potentially contributing to the d

89 us protein (VP)40, administered 1-3 d before Ebola virus infection rapidly induced protective immunit

90 haracterization of the ferret as a model for Ebola virus infection, reproducing disease and lethality

91 Our findings provide insights into Ebola virus infection that could be exploited for the de

92 expected number of internationally exported Ebola virus infections, the potential effect of air trav

93 ith vaccination response, and no evidence of Ebola virus infection was detected.

94 Ebola virus infection was more widespread in this spillo

95 e of 1182 patients with laboratory-confirmed Ebola virus infections was 52%.

96 A passive immunization strategy for treating Ebola virus infections was evaluated using BALB/ c mice,

97 to be increased in patients with fatal Zaire Ebola virus infection, were not increased in any of the

98 NK cells treated with VLPs protected against Ebola virus infection when adoptively transferred to nai

99 00% protection, respectively, against lethal Ebola virus infection when treatment is initiated 24 hou

100 from all patients with laboratory-confirmed Ebola virus infection who received care in U.S. and Euro

101 acterization of the pathophysiology of acute Ebola virus infection with host innate and adaptive immu

102 est Africa experienced the first epidemic of Ebola virus infection, with by far the greatest number o