ライフサイエンスコーパス: TBEV

1 TBEV acutely infects the central nervous system (CNS), l

2 TBEV is endemic in northern Asia and Europe; however, du

3 TBEV/DEN4Delta30 and YF 17D demonstrated remarkably simi

4 LRP8's role as a TBEV receptor has implications for TBEV neuropathogenesi

5 ptor with high expression in the brain, as a TBEV receptor.

6 Substitutions were made within a TBEV reverse genetic system and recovered mutants were c

7 rate-binding antiviral agents active against TBEV.

8 monoclonal antibodies are protective against TBEV, but little is known about the human antibody respo

9 ly help to design a targeted therapy against TBEV.

10 cal testing was negative for Borreliosis and TBEV.

11 y additional viruses, such as mpox virus and TBEV.

12 only marginally affected ZIKV, WNV, YFV, and TBEV replication, while DENV titers were strongly reduce

13 izing antibodies against LGT TP21 as well as TBEV and were completely protected against subsequent LG

14 vations for development of a live attenuated TBEV vaccine are discussed.

15 for further development of a live attenuated TBEV vaccine.

16 vaccine candidate against disease caused by TBEV.

17 evaluation in mice and monkeys, the chimeric TBEV/DEN4Delta30 virus, carrying the prM and E protein g

18 mpared the neuropathogeneses of the chimeric TBEV/DEN4Delta30 virus; Langat virus (LGTV), a former li

19 sights into the NK cell response to clinical TBEV infection.

20 Although effective TBEV vaccines have been approved, vaccination coverage i

21 e encephalitis, and tick-borne encephalitis (TBEV) viruses are important neurotropic human pathogens,

22 No therapeutics are currently available for TBEV-associated disease.

23 role as a TBEV receptor has implications for TBEV neuropathogenesis and the development of antiviral

24 at this modulatory role may be important for TBEV survival in nature, where the virus circulates by n

25 o called ApoER2) as a candidate receptor for TBEV strains from the five different subtypes.

26 However, the entry receptors for TBEV, which contribute to cell and tissue tropism, remai

27 -borne RNA viruses-host factors required for TBEV entry remain poorly defined.

28 Genetic ablation of LRP8 impaired TBEV reporter virus particle or authentic virus infectio

29 IMPORTANCE TBEV infection may result in encephalitis, chronic illne

30 and additive action of endogenous IFITMs in TBEV suppression.

31 Our studies establish a role for LRP8 in TBEV entry and infection, which has implications for the

32 no studies on the role of IFITM proteins in TBEV infection have been published thus far.

33 elated and more pathogenic viruses including TBEV, Louping ill virus, Omsk hemorrhagic fever virus (O

34 tion or ectopic expression of LRP8 increased TBEV infection.

35 Work with infectious TBEV requires high-level biocontainment, meaning model s

36 euronal cells and protected mice from lethal TBEV challenge.

37 ted extensively in clinical trials as a live TBEV vaccine and was found to induce a protective, durab

38 30 virus; Langat virus (LGTV), a former live TBEV vaccine; and yellow fever 17D virus vaccine (YF 17D

39 Soluble LRP8-Fc decoy receptors neutralized TBEV in cell culture, and reduced viral infection was ob

40 Nevertheless, TBEV/DEN4Delta30 virus exhibited higher neurovirulence i

41 eration of a self-replicating, noninfectious TBEV replicon used to study properties of high (Hypr) an

42 Here, we described the construction of novel TBEV replicons that permit a molecular comparison of TBE

43 We describe a new association of TBEV with uveitis.

44 the differential clinical characteristics of TBEV strains.

45 Characterization of TBEV isolates is challenging due to the requirement for

46 licons that permit a molecular comparison of TBEV isolates of high and low pathogenicity.

47 ty of an effective vaccine, the incidence of TBEV is increasing worldwide.

48 TM1, IFITM2, and IFITM3 in the inhibition of TBEV infection and in protection against virus-induced c

49 role of IFITM proteins in the inhibition of TBEV infection and virus-mediated cell death.

50 chemokine receptor Ccr5 in a mouse model of TBEV infection using the naturally attenuated tick-borne

51 rovirulence and abolish neuroinvasiveness of TBEV, namely substitution of structural protein genes of

52 The pathology of TBEV ranges from mild to fatal, depending on the virus g

53 In contrast, the profile of TBEV grown in tick cells showed that paucimannose (Man(3

54 file of N-glycans linked to the E protein of TBEV when grown in human neuronal cells and compare it t

55 ed with the highly virulent Sofjin strain of TBEV.

56 as used as a receptor by multiple strains of TBEV and several closely related tick-borne viruses but

57 ne-linked oligosaccharides on the surface of TBEV derived from human neuronal cells.

58 uctural protein genes of a highly pathogenic TBEV.

59 rties of high (Hypr) and low (Vs) pathogenic TBEV isolates.

60 LRP8 downregulation reduced TBEV infection in human cells, and its overexpression en

61 However, our data suggest that TBEV cell-to-cell spread may be less prone to both inter

62 the results of coculture assays suggest that TBEV might partially escape interferon- and IFITM-mediat

63 ntified two separate clines, suggesting that TBEV spread both east and west from a central point.

64 ot observed in any of these systems, and the TBEV and WNV systems did not yield any viable recombinan

65 r-128a, mir-218, or let-7c microRNA into the TBEV/DEN4 genome was sufficient to prevent the developme

66 N-Glycosylation of the TBEV envelope (E) glycoprotein is critical for virus egr

67 This highlights the utility of the TBEV replicons for further virological characterization

68 (LGTV), a naturally attenuated member of the TBEV serogroup.

69 A seroconversion of the TBEV- immunoglobulin titres was observed 2 weeks later w

70 LRP8 bound directly to the TBEV E glycoprotein and mediated viral attachment and in

71 This TBEV-induced NK cell activation was restricted predomina

72 mans by mosquitos (WNV, USUV, RRV) or ticks (TBEV, POWV).

73 LRP8 bound directly to TBEV envelope proteins and promoted virus attachment to

74 indings demonstrate that NK cells respond to TBEV infection with characteristics that are distinct fr

75 the human neutralizing antibody response to TBEV in a cohort of infected and vaccinated individuals.

76 al analysis of the human NK cell response to TBEV infection in a cohort of infected individuals from

77 i.p. 50% lethal doses of the highly virulent TBEV.

78 imeric tick-borne encephalitis/dengue virus (TBEV/DEN4) that contained the structural protein genes o

79 Tick-borne encephalitis virus (TBEV) causes tick-borne encephalitis (TBE), a severe and

80 embers of the tick-borne encephalitis virus (TBEV) complex, was firstly isolated from Ixodes granulat

81 member of the tick-borne encephalitis virus (TBEV) complex, was tested extensively in clinical trials

82 Tick-borne encephalitis virus (TBEV) is a flavivirus that is transferred to humans by i

83 Tick-borne encephalitis virus (TBEV) is a vector-transmitted flavivirus that causes pot

84 Tick-borne encephalitis virus (TBEV) is an emerging human pathogen that causes potentia

85 IMPORTANCE Tick-borne encephalitis virus (TBEV) is an emerging virus of the flavivirus family that

86 Tick-borne encephalitis virus (TBEV) is an important human arthropod-borne virus that c

87 Tick-borne encephalitis virus (TBEV) is the causative agent of severe human neuroinfect

88 Tick-borne encephalitis virus (TBEV) is the most medically relevant tick-transmitted Fl

89 ern strain of tick-borne encephalitis virus (TBEV) on the backbone of a nonneuroinvasive dengue type

90 Tick-borne encephalitis virus (TBEV), a member of the Flaviviridae family, is a leading

91 Tick-borne encephalitis virus (TBEV), of the genus Flavivirus, is a causative agent of

92 sociated with tick-borne encephalitis virus (TBEV), the most virulent of the tick-borne flaviviruses.

93 derived from tick-borne encephalitis virus (TBEV), West Nile virus (WNV), and Japanese encephalitis

94 with those of tick-borne encephalitis virus (TBEV), yellow fever virus (YFV), and Japanese encephalit

95 most virulent tick-borne encephalitis virus (TBEV).

96 er (YFV), and tick-borne encephalitis virus (TBEV).

97 apsid gene of tick-borne encephalitis virus (TBEV, genus Flavivirus).

98 tral nervous system caused by the TBE virus (TBEV), which is usually transmitted by a tick-bite, with

99 Tick-borne encephalitis (TBE) virus (TBEV) is transmitted to humans via tick bites.

100 k-borne encephalitis (TBE, due to TBE virus [TBEV]) (~10%).

101 aviviruses, tick-borne encephalitis viruses (TBEV) are an antigenic group that causes severe neurolog

102 studies on tick-borne encephalitis viruses (TBEV), based on partial envelope gene sequences, predict

103 ses in mice that were lethally infected with TBEV.

104 arboviral diseases due to Flaviviridae (WNV, TBEV, POWV, USUV) or Togaviridae (RRV) viruses transmitt