ライフサイエンスコーパス: WNV

1 WNV has caused over 18,000 cases of neuroinvasive diseas

2 WNV induces a significant antibody response that remains

3 WNV NS2B/3 cleavage of the DENV structural polyprotein w

4 WNV uses programmed -1 ribosomal frameshifting (-1 PRF)

5 WNV-NS5-E218A-recovered mice (recovery defined as surviv

6 roduction and outcome of infection among 115 WNV-positive US blood donors identified in 2008-2011.

7 ican WNV-like Koutango virus (WNVKOU), and a WNV-like isolate from Sarawak, Malaysia (WNVSarawak), we

8 Inoculation of WNV-NS5-E218A, a WNV with a mutant NS5(E218A) protein leads to survival r

9 l role of IVIG therapy in controlling active WNV infection, particularly in immunosuppressed patients

10 tralian strain, Kunjin (WNVKUN), the African WNV-like Koutango virus (WNVKOU), and a WNV-like isolate

11 ithin the central nervous system (CNS) after WNV infection, leading to entry of activated peripheral

12 s, which were differentially expressed after WNV NY99 and WNV Eg101 infections, respectively, and 147

13 ll death/apoptosis were only expressed after WNV NY99 infection.

14 3 expression was not stably maintained after WNV infection in MAVS-deficient mice.

15 kines generated in MAVS-deficient mice after WNV infection.

16 ntially expressed genes indicated that after WNV NY99 infection, TREM-1 mediated activation of toll-l

17 ARs) in which the antiviral activity against WNV and DENV hinges largely on both the 5'-silyl group a

18 hich turns on the antiviral activity against WNV and DENV while abrogating the previously reported an

19 promoting CD8(+) T cell cytotoxicity against WNV infection in mice.

20 iate a robust innate immune response against WNV infection in the absence of infiltrating inflammator

21 left intact, depleted, or stimulated against WNV.

22 lta T cell expansion, and lower antibody and WNV-specific T cell responses in old mice.

23 In comparison, when DENV and WNV were produced in insect cells, they also infected HU

24 Using convalescent plasma from DENV- and WNV-infected individuals, we found substantial enhanceme

25 ecimens from patients with confirmed JEV and WNV infections and compared the results with prM/E conta

26 able result for the serodiagnosis of JEV and WNV infections without the need for PRNT.

27 from patients with confirmed DENV, JEV, and WNV infections, along with naive sera, were subjected to

28 ommon and specific responses to WNV NY99 and WNV Eg101 infections as well as genes linked to potentia

29 differentially expressed after WNV NY99 and WNV Eg101 infections, respectively, and 147 genes were c

30 West Nile virus (WNV) NY99 (pathogenic) and WNV Eg101 (non-pathogenic) strains.

31 we observed generation of an effective anti-WNV immune response when Tregs lacked MAVS, thereby demo

32 required for participation of Tregs in anti-WNV immunity.

33 the mechanism by which flaviviruses such as WNV translate their genomes in host cells is incompletel

34 In a dual-luciferase reporter assay, WNV NS1 significantly inhibited the activation of the IF

35 0 value of 3.4 muM at DENV-2 and 15.5 muM at WNV for the most active analogue.

36 Recent work showed that an attenuated WNV, a nonstructural (NS) 4B-P38G mutant, induced no let

37 ate the protective efficacy of an attenuated WNV, the nonstructural 4B-P38G mutant, which was previou

38 t immune cells of the CNS, were activated by WNV infection, as exemplified by their amoeboid morpholo

39 that populations were negatively affected by WNV in 23 of the 49 species studied (47%).

40 Of interest, IFNgamma(+) and CD69(+) WNV-primed T cells were able to overcome CXCL12-mediated

41 on response appears to be crucial to control WNV infection, successful immunity may require a modest

42 rtantly, we demonstrate that sfRNA-deficient WNV displays significantly decreased infection and trans

43 An sfRNA1-deficient WNV was generated that displayed growth kinetics similar

44 resulted in increased mortality and delayed WNV clearance from the brain.

45 the replication of three flaviviruses, DENV, WNV, and Japanese encephalitis virus (JEV), using a high

46 ith a wide range of viruses, including DENV, WNV, yellow fever virus, Sindbis virus, Venezuelan equin

47 Here we develop a model depicting WNV transmission dynamics, which we optimize using a dat

48 n WNV lineage 1 circulated in Israel, as did WNV lineage 2, highlighting a high genetic diversity of

49 However, the role of IL-17A during WNV infection remains unclear.

50 ry of CXCR4(+) virus-specific T cells during WNV infection.

51 cellular infiltrate found in the CNS during WNV encephalitis, although the molecular cues involved i

52 inocycline reduces viral cytotoxicity during WNV infection in ex vivo CNS tissue.IMPORTANCE West Nile

53 bits TLR7-mediated antiviral immunity during WNV infection in mice.

54 an enhanced vulnerability in old mice during WNV NS4B-P38G mutant infection.

55 ically and in the draining lymph node during WNV infection.

56 an target of rapamycin (mTOR) pathway during WNV infection was not well understood.

57 Proinflammatory responses during WNV infection have been extensively studied, but anti-in

58 we investigated the function of sfRNA during WNV infection of Culex pipiens mosquitoes and evaluated

59 ted neurons and presynaptic terminals during WNV neuroinvasive disease.

60 ombined, our experiments suggest that during WNV infection, Ccr7 is a gatekeeper for nonspecific vira

61 nal involved in leukocyte trafficking during WNV infection, and it may have therapeutic potential for

62 Efficient WNV clearance and moderate susceptibility to WNV-mediate

63 overall results suggest that OPN facilitates WNV neuroinvasion by recruiting WNV-infected PMNs into t

64 optimization resulted in a final six-feature WNV model, which can predict hybridization rate constant

65 As a member of the family Flaviviridae, WNV is part of a group of clinically important human pat

66 Following WNV infection of primary neurons, we found that Asyn pro

67 aling are upregulated in the brain following WNV infection.

68 ctive and reparative capabilities) following WNV infection have not been investigated.

69 ulated gene-56 and Tlr7 expression following WNV infection.

70 fection, Israel serves as a resource hub for WNV in Africa and Eurasia and provides valuable informat

71 or was positive for WNV IgM but negative for WNV RNA, whereas his lymph node and spleen tissues teste

72 node and spleen tissues tested positive for WNV by RT-PCR.

73 Serum from the organ donor was positive for WNV IgM but negative for WNV RNA, whereas his lymph node

74 c targets and develop effective vaccines for WNV infections.

75 he NS1' frameshift signals derived from four WNV strains were investigated to better understand -1 PR

76 higher risk of neurologic complications from WNV infection.

77 ith various levels of genetic diversity from WNV were substituted.

78 Hippocampi from WNV-NS5-E218A-recovered mice with poor spatial learning

79 zation could not protect Mavs(-/-) mice from WNV-induced lethal disease.

80 determined that Ifi27l2a protects mice from WNV-induced mortality by contributing to the control of

81 we determined that Ifitm3 protects mice from WNV-induced mortality by restricting virus accumulation

82 ement C3 or C3a receptor were protected from WNV-induced synaptic terminal loss.

83 itive impairment in patients recovering from WNV neuroinvasive disease.

84 Furthermore, WNV NS1 inhibits the K63-linked polyubiquitination of RI

85 and Cx. quinquefasciatus exhibiting greater WNV divergence.

86 lls and peripheral organs in the two groups, WNV-infected polymorphonuclear neutrophil (PMN) infiltra

87 trospective ensemble forecasts of historical WNV outbreaks in Long Island, New York for 2001-2014.

88 redict spillover transmission risk and human WNV cases remains limited.

89 Murine and human WNV neuroinvasive disease post-mortem samples exhibit lo

90 and cognitive dysfunction that mirror human WNV neuroinvasive disease.

91 Predictions were accurate for cases of human WNV infection in the following year (2012), with areas r

92 mosquito infection rates and reported human WNV cases.

93 asts accurately predict seasonal total human WNV cases up to 9 weeks before the past reported case.

94 with the host antiviral response.IMPORTANCE WNV Nile virus (WNV) has received increased attention si

95 val of neurons, microglia, and astrocytes in WNV-infected slices and markedly decreased levels of ind

96 alyze global differential gene expression in WNV-infected mice brain and to identify the host cellula

97 e pattern of differential gene expression in WNV-infected, compared to uninfected, brains.

98 ptosis as a pathway that may be important in WNV pathogenesis, based on the pattern of differential g

99 (CNS) and host-factors that are involved in WNV neuroinvasion are not completely understood.

100 activation of CNS macrophages (microglia) in WNV-infected SCSC while inhibiting the expression of gen

101 To address these key questions in WNV evolution and ecology, we sequenced the complete gen

102 in cells, analysis of the immune response in WNV-infected Ifitm3(-/-) mice showed decreases in the to

103 There was a resurgence in WNV disease in the United States in 2012.

104 , suggesting OPN plays a deleterious role in WNV infection.

105 lammatory mechanisms may also play a role in WNV-induced pathology and/or recovery.

106 velopment of a greater number of symptoms in WNV-infected individuals.

107 ains of Opn (-/-) mice resulted in increased WNV-infected PMN infiltration and viral burden in the br

108 mmon donor residing in a region of increased WNV activity.

109 During systemic mosquito infection, WNV faced stochastic reductions in genetic diversity tha

110 ion experiments showed that Ifitm3 inhibited WNV infection independently of Ifitm1, Ifitm2, Ifitm5, a

111 AZT) consistently and selectively inhibiting WNV and DENV at low micromolar concentrations.

112 Interestingly, WNV-infected OPN deficient (Opn (-/-)) mice exhibited a

113 strate that IL-17A protects mice from lethal WNV infection by promoting CD8(+) T cell-mediated cleara

114 cells is critical for protection from lethal WNV infection.

115 tm3(-/-) mice were more vulnerable to lethal WNV infection, and this was associated with greater viru

116 king Ifi27l2a were more vulnerable to lethal WNV infection, the viral burden was greater only within

117 Mechanistically, WNV NS1 targets RIG-I and melanoma differentiation-assoc

118 e mosquito survey was established to monitor WNV activity and characterize viral genotypes in Israel.

119 ination of presynaptic terminals in a murine WNV neuroinvasive disease model.

120 al fragment (residues 172-352) of West Nile (WNV) and Dengue virus NS1 proteins at 1.85 and 2.7 A res

121 s (HEV), dengue virus (DENV), and West Nile (WNV) virus infection in blood plasma.

122 nt with this observation, only ZIKV, but not WNV or DENV, bound the AXL ligand Gas6.

123 Although thousands of cases of WNV-mediated memory dysfunction accrue annually, the mec

124 romoting CD8(+) T cell-mediated clearance of WNV.

125 mmatory responses are a crucial component of WNV pathology, and understanding how they are regulated

126 cerebellum and brain stem, in the context of WNV infection, a deficiency of Ifi27l2a was associated w

127 responses, which are critical for control of WNV infection, are initiated by signaling through pathog

128 e and genetic factors involved in control of WNV infection, no specific therapy is yet available.

129 Diagnosis was made based on detection of WNV IgM in the serum.

130 , the pattern, dynamics, and determinants of WNV spread in its natural hosts remain uncertain.

131 Projected geographic distributions of WNV in North America under future climate for 2050 and 2

132 2, highlighting a high genetic diversity of WNV genotypes in our region.

133 ary factor(s) responsible for enhancement of WNV replication.

134 the mechanism responsible for enhancement of WNV replication.

135 administration necessary for enhancement of WNV viremia using a mouse model.

136 In sum, the molecular evolution of WNV in North America depicts a largely unfettered expans

137 Inoculation of WNV-NS5-E218A, a WNV with a mutant NS5(E218A) protein le

138 opoietic cells in augmenting the kinetics of WNV clearance and thereby preventing a dysregulated and

139 ficient mice resulted in increased levels of WNV in the CNS, thereby effectively contributing to neur

140 r dendritic cells sustained higher levels of WNV infection than wild-type cells and that this differe

141 nd radiosensitive cells, as higher levels of WNV were observed in the brain only when Ifitm3 was abse

142 variability associated with the majority of WNV infections, we evaluated the association of cytokine

143 wo decades and a recently developed model of WNV risk, we estimated the impact of this emergent disea

144 Our study provides a new murine model of WNV-induced spatial memory impairment, and identifies a

145 Mouse models of WNV infection demonstrate that a proinflammatory environ

146 Experimental mouse models of WNV infection have established the importance of innate

147 ed that the nonstructural protein 1 (NS1) of WNV antagonizes IFN-beta production, most likely through

148 ed that the nonstructural protein 1 (NS1) of WNV antagonizes the induction of interferon beta (IFN-be

149 Outbreaks of WNV infection tend to be unpredictable, and a safe and e

150 real-time forecast of seasonal outbreaks of WNV.

151 herapeutically alter the survival outcome of WNV infection, we administered exogenous CCL7 i.v. to WN

152 s of EIII to the tropism and pathogenesis of WNV or other flaviviruses.

153 opodia and lamellipodia, and phagocytosis of WNV-infected cells and debris.

154 eonine were tolerated at the P1' position of WNV capsid.

155 ating that Treg detection of the presence of WNV through the MAVS signaling pathway is not required f

156 n this article, studies of the processing of WNV and DENV capsid proteins by the WNV protease identif

157 provides new insights into the regulation of WNV NS1 in the RLR signaling pathway and reveals a novel

158 to saliva and SGE enhance the replication of WNV.

159 act (SGE) enhance the in vivo replication of WNV.

160 contributes to innate immune restriction of WNV in a cell-type- and tissue-specific manner.

161 ulin M, and occasionally positive results of WNV-specific real-time reverse-transcription polymerase

162 years and, here, report partial sequences of WNV genomes obtained from 102 of the 336 positive mosqui

163 Small-RNA deep sequencing of WNV-infected mosquitoes indicated an active small interf

164 ent options useful in limiting the spread of WNV, other mosquito-borne viruses, and the diseases that

165 TCRm staining of WNV-infected cells demonstrated that the immunorecessive

166 determined the 3.0 A resolution structure of WNV NS1(172-352) with the protective 22NS1 antibody Fab,

167 The infectious titer of WNV and Venezuelan equine encephalitis virus (VEEV) TC83

168 In addition, treatment of WNV-infected mice with recombinant IL-17A reduces the vi

169 vitro and in vivo Importantly, treatment of WNV-infected mice with recombinant IL-17A, as late as da

170 dendritic cells resulted in higher yields of WNV in multistep growth analyses.

171 Eurasia and provides valuable information on WNV circulation in these regions.

172 th much greater efficiency than does DENV or WNV.

173 Administration of DENV- or WNV-convalescent plasma into ZIKV-susceptible mice resul

174 JEV or WNV was reliably identified as the currently infecting f

175 tionally affected by temporary or persistent WNV effects, suggesting an evolutionary dimension of dis

176 As predicted, WNV diversity was significantly lower in RNAi-depleted c

177 ted 124 patients with a diagnosis of primary WNV infection (PI) or NPI during 2005-2007 at Sheba Medi

178 facilitates WNV neuroinvasion by recruiting WNV-infected PMNs into the brain.

179 ) T cell recall response, a modestly reduced WNV-specific IgM production, but more robust CD8(+) T ce

180 on of mTOR (KU0063794) significantly reduced WNV growth.

181 Our data suggest that Ifitm3 restricts WNV pathogenesis by multiple mechanisms and functions in

182 Our analyses suggest that Ifitm3 restricts WNV pathogenesis likely through multiple mechanisms, inc

183 ) encephalitis, we show that RIPK3 restricts WNV pathogenesis independently of cell death.

184 ious studies have phylogenetically separated WNV strains into two main genetic lineages (I and II) co

185 Several WNV-like strains clustering outside these lineages have

186 We report three cases of severe WNV infection complicated by meningoencephalitis in our

187 This suggests that specific WNV vector-bird species pairings may generate novel geno

188 ees of pathogenesis associated with specific WNV strains.

189 3 protein)-and used these TCRm mAbs to stain WNV-infected cell lines and primary APCs.

190 etics of currently circulating United States WNV strains do not explain variations in epidemic magnit

191 n of the host mechanisms required to support WNV genome translation will provide broad understanding

192 n of ER signaling pathways, known to support WNV replication, were significantly elevated before and

193 ral lineages are of similar fitness and that WNV is well adapted to the ecology of mosquito vectors a

194 We previously demonstrated that WNV infection of mice deficient in mitochondrial antivir

195 In this study, we found that WNV infection induced OPN expression in both human and m

196 Thus, our results indicate that WNV-induced neuronal injury in the brain is mediated by

197 Grubaugh et al. observed that WNV genetic divergence is dependent on the vector mosqui

198 We now show that WNV activates mTOR and cognate downstream activators of

199 enomes sampled from wild birds, we show that WNV experienced an explosive spread with little geograph

200 In mice, we previously showed that WNV infection induces a CCR2-dependent monocytosis that

201 Our previous work has shown that WNV growth was independent of macroautophagy activation,

202 l replication in this organ, suggesting that WNV may migrate from the skin into the lymph node throug

203 inhibitor of neuroinflammation, altered the WNV-induced proinflammatory cytokine/chemokine expressio

204 lues of 12 nM at the DENV-2 and 39 nM at the WNV proteases.

205 ssing of WNV and DENV capsid proteins by the WNV protease identified an unexpected contribution of th

206 regulating the inflammatory response in the WNV-infected brain.

207 laviviruses were substituted in place of the WNV EIII were recovered, although the substitution of se

208 uct could be achieved in the presence of the WNV NS2B-3 protease, which cleaves C from prM, allowing

209 in defining the cleavage specificity of the WNV protease.

210 We now show that the WNV-induced expression of these and other proinflammator

211 acy during immunization of old mice with the WNV NS4B-P38G mutant.

212 Further application of the assays to WNV- and JEV-infected serum panels showed similar result

213 deficient (Tlr8(-/-)) mice were resistant to WNV infection compared with wild-type controls.

214 e a proinflammatory phenotype in response to WNV infection similar to the proinflammatory (M1) activa

215 environment and cytotoxicity in response to WNV infection without peripheral immune cell involvement

216 tified both common and specific responses to WNV NY99 and WNV Eg101 infections as well as genes linke

217 WNV clearance and moderate susceptibility to WNV-mediated neuronal death in Tlr8(-/-) mice were attri

218 nt (Il17a(-/-)) mice are more susceptible to WNV infection and develop a higher viral burden than wil

219 d (21- to 22-month) mice were susceptible to WNV NS4B-P38G mutant infection but were protected from s

220 tion, we administered exogenous CCL7 i.v. to WNV-infected Ccl7(-/-) mice and observed a significant i

221 cting flavivirus by a higher ratio of JEV-to-WNV P/N values or vice versa.

222 e protected from subsequent lethal wild-type WNV challenge.

223 rowth kinetics similar to those of wild-type WNV in both RNA interference (RNAi)-competent and -compr

224 d host protection during secondary wild-type WNV infection.

225 le-tube duplex detection of West Nile virus (WNV) and chikungunya virus (CHIKV) RNA.

226 West Nile virus (WNV) and Dengue virus (DENV) are important human pathoge

227 West Nile virus (WNV) and dengue virus (DENV) are mosquito-borne flavivir

228 ead of flaviviruses such as West Nile virus (WNV) and Zika virus, it is critical that we develop a co

229 West Nile virus (WNV) can cause severe human neurological diseases includ

230 une plasma against DENV and West Nile virus (WNV) can enhance Zika virus (ZIKV) infection and pathoge

231 vivo CNS tissue.IMPORTANCE West Nile virus (WNV) causes substantial morbidity and mortality, with no

232 irus dengue virus (DENV) or West Nile virus (WNV) does not result in the production of any virus-deri

233 The arthropod-borne West Nile virus (WNV) emerged in New York State in 1999 and quickly sprea

234 Using a mouse model of West Nile virus (WNV) encephalitis, we show that RIPK3 restricts WNV path

235 The West Nile Virus (WNV) envelope protein, E, promotes membrane fusion durin

236 iously reported a series of West Nile virus (WNV) epitopes that are naturally presented by HLA-A*02:0

237 euroinvasive infection with West Nile virus (WNV) exhibit chronic cognitive sequelae.

238 n to North America in 1999, West Nile virus (WNV) has had devastating impacts on native host populati

239 ntiviral response.IMPORTANCE WNV Nile virus (WNV) has received increased attention since its introduc

240 ergence of the vector-borne West Nile virus (WNV) in North America in 1999 represents a classic examp

241 cipients with donor-derived West Nile virus (WNV) infection (encephalitis 3, asymptomatic 1) from a c

242 critical for the control of West Nile virus (WNV) infection by regulating type I IFN (IFN-I) response

243 cal picture consistent with West Nile virus (WNV) infection, which was defined as nonprimary infectio

244 +) T cells in recovery from West Nile virus (WNV) infection.

245 vital role in recovery from West Nile virus (WNV) infection.

246 ncephalitis virus (JEV) and West Nile virus (WNV) infections is the premembrane/envelope (prM/E)-spec

247 es were generated using the West Nile virus (WNV) infectious clone, into which EIIIs from nine flaviv

248 The introduction of West Nile virus (WNV) into North America in 1999 is a classic example of

249 West Nile virus (WNV) is a major cause of mosquito-borne illness in the U

250 West Nile virus (WNV) is a mosquito-borne flavivirus that causes epidemic

251 West Nile virus (WNV) is a mosquito-transmitted flavivirus that can cause

252 West Nile virus (WNV) is a neurotropic flavivirus that can cause signific

253 West Nile virus (WNV) is a neurotropic flavivirus that causes significant

254 West Nile virus (WNV) is a neurotropic ssRNA flavivirus that can cause en

255 West Nile virus (WNV) is a prototypical emerging virus for which no effec

256 West Nile virus (WNV) is a re-emerging pathogen and the leading cause of

257 West Nile virus (WNV) is an emerging cause of meningitis and encephalitis

258 West Nile Virus (WNV) is endemic in Israel and has been the cause of seve

259 West Nile virus (WNV) is now endemic in the continental United States; ho

260 West Nile virus (WNV) is the most important cause of epidemic encephaliti

261 West Nile virus (WNV) is the most important cause of mosquito-transmitted

262 West Nile virus (WNV) nonstructural (NS) 4B-P38G mutant has several featu

263 The dengue virus (DENV) and West Nile Virus (WNV) NS2B-NS3 proteases are attractive targets for the d

264 of distinct pathologies of West Nile virus (WNV) NY99 (pathogenic) and WNV Eg101 (non-pathogenic) st

265 stigated how IRF5 modulates West Nile virus (WNV) pathogenesis and host immune responses.

266 irus genomes, we quantified West Nile virus (WNV) quasispecies diversity after passage in Drosophila

267 West Nile virus (WNV) remains an important public health problem causing

268 n (GFP) reporter-expressing West Nile virus (WNV) replicon.

269 While a West Nile virus (WNV) subgenomic RNA could readily be packaged by structu

270 against the live attenuated West Nile virus (WNV) vaccine strain, the nonstructural (NS) 4B-P38G muta

271 Several viable West Nile virus (WNV) variants with chimeric E proteins in which the puta

272 a history of infection with West Nile virus (WNV), (ii) 34 healthy subjects of different ages.

273 West Nile virus (WNV), a mosquito-borne flavivirus, has induced severe ne

274 West Nile virus (WNV), an emerging mosquito-borne flavivirus, has induced

275 that restricts infection by West Nile virus (WNV), an encephalitic flavivirus of global concern.

276 s an antiviral gene against West Nile virus (WNV), an encephalitic flavivirus, in cells and mice.

277 activity of Ifitm3 against West Nile virus (WNV), an encephalitic flavivirus, using mice with a targ

278 viruses (DENV-1 to DENV-4), West Nile virus (WNV), and Japanese encephalitis virus (JEV), were constr

279 luding dengue virus (DENV), West Nile virus (WNV), and Zika virus (ZIKV), highlight the importance of

280 er virus, dengue virus, and West Nile virus (WNV), are a serious concern for human health.

281 as dengue virus (DENV) and West Nile virus (WNV), are endemic.

282 ated dengue virus (DENV) or West Nile virus (WNV), can efficiently infect key placental barrier cells

283 eloped RNA viruses, such as West Nile virus (WNV), invade the CNS and cause encephalitis, yet little

284 -borne RNA viruses, such as West Nile virus (WNV), is facilitated by genetically complex virus popula

285 V-68) with influenza virus, West Nile virus (WNV), or vesicular stomatitis virus (VSV).

286 FV), Zika virus (ZIKV), and West Nile virus (WNV), profoundly affect human health.

287 fi27l2a during infection by West Nile virus (WNV).

288 Here, we report a weighted neighbour voting (WNV) prediction algorithm, in which the hybridization ra

289 Here, we determine whether WNV enzootic (Culex tarsalis, Cx. quinquefasciatus, and

290 The mechanisms by which WNV enters the central nervous system (CNS) and host-fac

291 thway and reveals a novel mechanism by which WNV evades the host innate immune response.

292 ur results reveal a novel mechanism by which WNV NS1 interferes with the host antiviral response.IMPO

293 ished two groups of species: those for which WNV negatively impacted survival only during initial spr

294 applied in areas where JEV cocirculates with WNV, or to 100% when applied in areas that were endemic

295 ilar to mouse models, infection of SCSC with WNV induces the upregulation of proinflammatory genes an

296 astern European subtypes of cluster 2 within WNV lineage 1 circulated in Israel, as did WNV lineage 2

297 priming were all protected from a lethal WT WNV challenge.

298 recall T cell responses during secondary WT WNV infection.IMPORTANCE The production of innate cytoki

299 , and protection of mice from wild-type (WT) WNV infection.

300 its introduction into the state of New York, WNV spread across the United States, reaching California