ライフサイエンスコーパス: JEV

1 JEV or WNV was reliably identified as the currently infe

2 JEV provides a paradigm for other flaviviruses, includin

3 JEV seroprevalence and annual infection estimates were m

4 We estimate in 2015 JEV infections caused 100,308 JE cases (95% CI: 61,720-1

5 Analysis of all 290 JEV isolates for which sequence data are available showe

6 Bangladesh is considering introducing a JEV vaccine; however, the investment case is hampered by

7 Moreover, a JEV DE mutant exhibited resistance to RC-101, which was

8 of JEV encephalitis, IRF8 modulation affects JEV replication.

9 well as superior antiviral activity against JEV infection.

10 icantly less neutralizing antibodies against JEV.

11 d the effect of preexisting immunity against JEV on subsequent dengue disease outcomes in a prospecti

12 g antibodies and protective immunity against JEV.

13 ers, not only to maintain protection against JEV in endemic regions but also to limit the potential o

14 le of T cell responses in protection against JEV, we conducted the first full-breadth analysis of the

15 ta suggest cross-protection between DENV and JEV.

16 e determined the molecular shapes of WNV and JEV SLAs and investigated WNV NS5 interaction with ortho

17 urther application of the assays to WNV- and JEV-infected serum panels showed similar results.

18 trocyclin-101 inhibited flavivirus (ZIKV and JEV) infections.

19 Discrimination between DENV/ZIKV and JEV/CHIKV was successfully demonstrated using real virus

20 hough WNV NS5 interacts with DENV, ZIKV, and JEV SLAs in binding assays, only DENV and ZIKV SLAs coul

21 The live-attenuated JEV SA14-14-2 vaccine has been vital for controlling the

22 ated JE-VAX and then boosted with attenuated JEV SA14-14-2.

23 The authentic JEV SA14-14-2 (E) protein, with amino acid substitutions

24 logy of acute encephalitis syndrome, besides JEV alone, and highlighted the importance of scrub typhu

25 mine whether there were associations between JEV immunity and dengue severity.

26 ntrolling the incidence of disease caused by JEV, particularly in rural areas of Asia where it is end

27 gies to treat and prevent diseases caused by JEV.

28 inflammatory cytokines/chemokines induced by JEV infection that inhibit the expression of TJ proteins

29 In addition, at 25 C, JEV disseminated from the midgut and was recovered in sa

30 contributions for six of the many candidate JEV-related host genes, including EMC3 and CALR.

31 However, with changing climate JEV has the potential to emerge in novel temperate regio

32 These data confirm JEV transmission across predominantly urban areas and su

33 serum specimens from patients with confirmed JEV and WNV infections and compared the results with prM

34 ed recombinant JEV (rJEV) strains containing JEV SA14-14-2 vaccine-specific mutations that are locate

35 specimens from patients with confirmed DENV, JEV, and WNV infections, along with naive sera, were sub

36 tudy in children aged 2-14 years to describe JEV endemicity, measuring antibodies by plaque reduction

37 Phylogenetic studies divided JEV into five geographically and epidemiologically disti

38 ed with displacement of GIII as the dominant JEV genotype throughout Asia in the 1990s.

39 nhanced vascular leakage in the brain during JEV infection is MC-dependent.

40 n infection and neurological deficits during JEV infection, and prolonged survival, suggesting chymas

41 mice display reduced BBB permeability during JEV infection compared to congenic wild-type (WT) mice,

42 ellow fever (YFV) and Japanese encephalitis (JEV) virus in different geographical regions.

43 (DENV), Zika (ZIKV), Japanese encephalitis (JEV), West Nile (WNV), and yellow fever (YFV) viruses by

44 y, chymase, a MC-specific protease, enhances JEV-induced breakdown of the BBB and cleavage of tight-j

45 ponsible for HSPGs sulfurylation, facilitate JEV entry into porcine cells.

46 ry to identify key host factors facilitating JEV infection in porcine cells.

47 when applied in areas that were endemic for JEV.

48 specificity of serodiagnosis, especially for JEV infection, was increased to 90% when applied in area

49 h, West Bengal, and Assam were evaluated for JEV (serum and cerebrospinal fluid [CSF] IgM ELISA) per

50 st that temperature is a critical factor for JEV vector competence and infected-mosquito survival.

51 at least 3.5 PFU/ml for YFV, 2.0 PFU/ml for JEV, 10.0 PFU/ml for WNV, and 10.0 PFU/ml for SLEV.

52 ral previously unreported genes required for JEV infection are highly enriched post-JEV selection.

53 amma (IFN-gamma) responses to JEV in healthy JEV-exposed donors were mostly CD8(+) and targeted nonst

54 However, JEV VLPs with KD or GKD mutations induced significantly

55 ntified as a potential target of miR-301a in JEV infection.

56 hallenge to mice and exhibit augmentation in JEV replication in the brain.

57 standing the mechanisms of BBB disruption in JEV infection is important.

58 t the expression of miR-301a is increased in JEV-infected microglial cells and human brain.

59 rated the enhancement of BBB permeability in JEV-infected mice, suggesting that IFN-gamma could be a

60 rated the enhancement of BBB permeability in JEV-infected mice.

61 Moreover, MCs promoted increased JEV infection in the central nervous system (CNS), enhan

62 a 1:160 serum dilution capable of inhibiting JEV, were associated with heightened biomarkers of dengu

63 Here, using a mouse model of intravenous JEV infection, we show that virus titers increased expon

64 -type (WT) VLP-immunized mice after a lethal JEV challenge.

65 fny(-/-) conferred protection against lethal JEV challenge to mice and exhibit augmentation in JEV re

66 mouse of MAb B2 1 day after otherwise lethal JEV infection protected 50% of mice and significantly pr

67 d one or two doses of DNA vaccine maintained JEV-specific antibodies 18 months after initial immuniza

68 rus dengue virus (DENV) cocirculates in many JEV-endemic areas, and clinical data suggest cross-prote

69 t al. report the cryo-EM structure of mature JEV at near-atomic resolution and identify structural el

70 Sera from JENVAC subjects neutralized JEV genotypes I, II, III, and IV equally well.

71 Furthermore, it is not JEV infection per se, but the inflammatory cytokines/che

72 GIII has been the source of numerous JEV epidemics throughout history and was the most freque

73 5% confidence interval (CI):17.1 to 21.1] of JEV antibodies.

74 D) mutations altered the binding activity of JEV VLP to cross-reactive monoclonal antibodies but had

75 by a limited understanding of key aspects of JEV ecology.

76 ollow-up studies to verify the dependency of JEV on these genes, and identify functional contribution

77 dult mice that had received a single dose of JEV DNA vaccine when 3 days of age were completely prote

78 nese encephalitis virus (JEV), the effect of JEV immunity on dengue disease severity is largely unkno

79 donesia-Malaysia region has all genotypes of JEV circulating, whereas only more recent genotypes circ

80 cs, we comprehensively defined the impact of JEV SA14-14-2 mutations on attenuation of virulence and

81 fourteen days, there were reduced levels of JEV dissemination and virus was not detected in saliva s

82 However, the mechanisms of JEV penetration of the blood-brain-barrier (BBB) remain

83 ll, we summarize that in the murine model of JEV encephalitis, IRF8 modulation affects JEV replicatio

84 ses linked to different clinical outcomes of JEV infection, associated with distinct targeting and br

85 ort in Nepal, which has a high prevalence of JEV immunity and rapidly rising dengue virus (DENV) infe

86 nstration of antibody-mediated protection of JEV infection in vivo is provided using the mouse enceph

87 r-CQDs effectively bound to the E protein of JEV, preventing viral entry into the host cells.

88 ly infecting flavivirus by a higher ratio of JEV-to-WNV P/N values or vice versa.

89 and reliable result for the serodiagnosis of JEV and WNV infections without the need for PRNT.

90 izing activities against a broad spectrum of JEV genotype strains.

91 ent of JEV with Cur-CQDs, a mutant strain of JEV was evolved that did not support binding of Cur-CQDs

92 this study, we demonstrate that the TMDs of JEV NS2B participate in both viral RNA replication and v

93 ial therapeutic avenues for the treatment of JEV infection.

94 In addition, after continued treatment of JEV with Cur-CQDs, a mutant strain of JEV was evolved th

95 rban areas and support a greater emphasis on JEV case finding, diagnosis, and prevention.

96 However, the impact of IRF8 modulation on JEV replication remains elusive.

97 emonstrated the effect of IRF8 modulation on JEV replication, microglial activation, and immune cells

98 f the core protein unlike that seen in other JEV strains.

99 Pathologically, JEV infection causes an acute encephalopathy accompanied

100 A minimal estimate of pediatric JEV seroprevalence in dengue-naive individuals was 8.1%

101 were completely protected from a 50, 000-PFU JEV intraperitoneal challenge.

102 d for JEV infection are highly enriched post-JEV selection.

103 ase is a novel therapeutic target to prevent JEV encephalitis.

104 hat a recombinant plasmid DNA which produced JEV EPs in vitro is an effective vaccine.

105 ond-generation, live-attenuated, recombinant JEV vaccine candidates.

106 Here, we generated recombinant JEV (rJEV) strains containing JEV SA14-14-2 vaccine-spec

107 h this plasmid vector (JE-4B clone) secreted JEV-specific extracellular particles (EPs) into the cult

108 While monomeric in solution, JEV E assembles as an antiparallel dimer in the crystal

109 In enhanced surveillance, JEV IgM-negative specimens were additionally evaluated f

110 ver, brain extracts derived from symptomatic JEV-infected mice, but not from mock-infected mice, indu

111 Our data demonstrate that JEV gains entry into the CNS prior to BBB disruption.

112 This study demonstrated that JEV DII(FL) is crucial for eliciting potently neutralizi

113 We also observed that JEV infection induces classical activation (M1) of micro

114 Here, we report that JEV infection enhances IRF8 expression in the infected m

115 Here we show that JEV activates MCs, leading to the release of granule-ass

116 Taken together, our data suggest that JEV enters the CNS, propagates in neurons, and induces t

117 These results suggest that JEV originated from its ancestral virus in the Indonesia

118 The JEV envelope protein (E) facilitates cellular attachment

119 Using the recombination trap and the JEV system, we detected two aberrant recombination event

120 Overexpression of miR-301a augments the JEV-induced inflammatory response, whereas inhibition of

121 sters and not mice were also detected in the JEV SA-14-14-2 vaccine.

122 ammaretrovirus sequences was detected in the JEV vaccine using PCR.

123 he 2.1-A resolution crystal structure of the JEV E ectodomain refolded from bacterial inclusion bodie

124 Attenuation depends on the presence of the JEV SA14-14-2 E protein, as shown by the high neurovirul

125 introduced from PCR-amplified regions of the JEV SA14-14-2 genome.

126 E of YFV 17D are replaced with those of the JEV SA14-14-2 vaccine strain is under evaluation as a ca

127 The failure of the JEV SLA to support WNV replication suggests that efficie

128 ts are consistent with the production of the JEV vaccine in Syrian hamster cells.

129 ver, the present study demonstrates that the JEV fusion loop plays a critical role in eliciting prote

130 Thus, our study suggests that the JEV-induced expression of miR-301a positively regulates

131 t did not support binding of Cur-CQDs to the JEV envelope.

132 , indicating cross-neutralization within the JEV PRNT50 assay.

133 on, uniquely conserved histidines within the JEV serocomplex suggest that pH-mediated structural tran

134 ever, the majority of individuals exposed to JEV only develop mild symptoms associated with long-last

135 hese results suggest that waning immunity to JEV could enhance the severity of dengue disease.

136 potential of maintaining strong immunity to JEV through vaccine boosters, not only to maintain prote

137 e, CC006, that was specifically resistant to JEV, suggesting that both pan-flavivirus and virus-speci

138 vo interferon-gamma (IFN-gamma) responses to JEV in healthy JEV-exposed donors were mostly CD8(+) and

139 ults show that Cx. pipiens is susceptible to JEV infection at both temperatures.

140 veloped >25 years ago by passaging wild-type JEV strain SA14 in tissue cultures and rodents, with int

141 mutant fusion loop encoded by commonly used JEV vaccine strains on vaccine efficacy or safety after

142 We used JEV serological data from a multicountry Asian dengue va

143 Despite the existence of effective vaccines, JEV is responsible for an estimated 68,000 human cases a

144 pipiens to vector JEV genotype III at temperatures representative of those

145 vectorial capacity of Cx. pipiens to vector JEV genotype III in temperate areas.

146 itoneal challenge with 5,000 PFU of virulent JEV strain SA14.

147 ines, including Japanese encephalitis virus (JEV) (SA-14-14-2), varicella (Varivax), measles, mumps,

148 Although Japanese encephalitis virus (JEV) accounts for around 15% of reported cases, the aeti

149 irus (YFV), and Japanese encephalitis virus (JEV) and by comparing the resultant chimeric viruses gen

150 gnosis of acute Japanese encephalitis virus (JEV) and West Nile virus (WNV) infections is the prememb

151 inhibited both Japanese encephalitis virus (JEV) and Zika virus (ZIKV) infections.

152 ur genotypes of Japanese encephalitis virus (JEV) are presently recognized (representatives of genoty

153 Nile virus, and Japanese encephalitis virus (JEV) are widely used as serodiagnostic tests for presump

154 Using Japanese encephalitis virus (JEV) as a model, we performed a systematic mutagenesis a

155 ver virus (YFV)/Japanese encephalitis virus (JEV) chimera in which the structural proteins prM and E

156 otype I (GI) of Japanese encephalitis virus (JEV) has displaced genotype III (GIII) as the dominant v

157 of IRF8 during Japanese encephalitis virus (JEV) infection in the brain remains elusive.

158 Japanese encephalitis virus (JEV) invades the CNS, resulting in neuroinflammation, wh

159 ic flaviviruses.Japanese encephalitis virus (JEV) is a Flavivirus responsible for thousands of deaths

160 Japanese encephalitis virus (JEV) is a leading cause of viral encephalitis.

161 Japanese encephalitis virus (JEV) is a major threat to human health.

162 Japanese encephalitis virus (JEV) is a mosquito-borne zoonotic flavivirus that causes

163 Japanese encephalitis virus (JEV) is a zoonotic, mosquito-borne flavivirus, distribut

164 Japanese encephalitis virus (JEV) is the leading global cause of viral encephalitis.

165 newly emerging Japanese encephalitis virus (JEV) or Japanese encephalitis (JE) serocomplex virus.

166 a vital role in Japanese encephalitis virus (JEV) pathogenesis.

167 tors containing Japanese encephalitis virus (JEV) premembrane (prM) and envelope (E) genes were const

168 live-attenuated Japanese encephalitis virus (JEV) SA14-14-2 vaccine are attributed to mutations that

169 irus (WNV), and Japanese encephalitis virus (JEV) that could complement each other in trans and thus

170 e caused by the Japanese encephalitis virus (JEV) that is prevalent in Asia and the Western Pacific.

171 ive efficacy of Japanese encephalitis virus (JEV) virus-like particles (VLPs) in mice.

172 Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, is the main cause of

173 Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, represents the most s

174 Japanese encephalitis virus (JEV), although confined to Asia, causes about 35000-5000

175 virus (WNV) and Japanese encephalitis virus (JEV), POWV disease presentation is heterogeneous, and th

176 o virus (KOUV), Japanese encephalitis virus (JEV), St. Louis encephalitis virus (SLEV), and Bagaza vi

177 mpaigns against Japanese encephalitis virus (JEV), the effect of JEV immunity on dengue disease sever

178 DENV, WNV, and Japanese encephalitis virus (JEV), using a high-content immunofluorescence screen.

179 We diagnosed Japanese encephalitis virus (JEV), using antibody detection, culture of serum and CSF

180 irus (WNV), and Japanese encephalitis virus (JEV), were constructed.

181 er virus (YFV), Japanese encephalitis virus (JEV), West Nile virus (WNV), St.

182 Japanese encephalitis virus (JEV)-specific Fab antibodies were recovered by repertoir

183 irus (HCV), and Japanese encephalitis virus (JEV).

184 rus (ZIKV), and Japanese encephalitis virus (JEV).

185 rus (ZIKV), and Japanese encephalitis virus (JEV).

186 sease caused by Japanese encephalitis virus (JEV).

187 ates analyzed), Japanese encephalitis virus (JEV; one isolate analyzed) and Zika virus (ZIKV; 2 isola

188 eveloped using an Indian strain of JE virus (JEV).

189 Japanese encephalitis (JE) virus (JEV) is an important cause of encephalitis in children o

190 he most commonly identified aetiologies were JEV, scrub typhus (645 [18.5%] of 3489), and dengue viru

191 increased to 90% when applied in areas where JEV cocirculates with WNV, or to 100% when applied in ar

192 V/JEV Nakayama chimera derived from the wild JEV Nakayama strain.

193 CNS infections, 144 (26%) were infected with JEV (134 children and 10 adults).

194 studies revealed that direct infection with JEV could not induce changes in the permeability of brai

195 mosquito species that have been linked with JEV transmission.

196 NCE Neuroinvasive flaviviruses, such as WNV, JEV, and POWV, are transmitted to humans by mosquitoes o

197 fluorogenic probes (probes specific for YFV, JEV, WNV, and SLEV) and four previously published probes

198 the high neurovirulence of an analogous YFV/JEV Nakayama chimera derived from the wild JEV Nakayama

199 The chimera (YFV/JEV SA14-14-2, or ChimeriVax-JE) is less neurovirulent t

200 d in attenuation, a series of intratypic YFV/JEV chimeras containing either single or multiple amino

201 the E proteins of ChimeriVax-JE and the YFV/JEV Nakayama virus, four of which are predicted to be ne

202 estore the neurovirulence typical of the YFV/JEV Nakayama virus.