ライフサイエンスコーパス: WNV

1 WNV and ZIKV actively blocked STAT5 phosphorylation down

2 WNV containing a NS1 deletion (WNV-DeltaNS1) could be ef

3 WNV spatial distribution is mainly determined by the mov

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

5 WNV-86 targets an epitope in E domain II, and preferenti

6 WNV-DeltaNS1 appeared to be safe, as no replicative viru

7 WNV-DeltaNS1 was noninfectious in mice, even when IFNAR(

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

9 tive" or "possible Zika positive" in 8 of 12 WNV or DENV PRNT-positive samples and in 12 of 22 PRNT-s

10 variation in expression of IL-1ra and IL-2; WNV-infected donors demonstrated variation in expression

11 ss spectrometry (APMS) study to identify 259 WNV-interacting human proteins.

12 ho were reactive for RNA from DENV (n = 71), WNV (n = 52) or ZIKV (n = 44), and a control or non-infe

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

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

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

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

17 3 expression was not stably maintained after WNV infection in MAVS-deficient mice.

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

19 aff deficiency had increased mortality after WNV infection and decreased WNV-specific IgG and neutral

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

21 rofile together with a good activity against WNV for which no treatments are currently available, mak

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

23 e protection, and immune programming against WNV infection.

24 ontributes to the antiviral response against WNV and identify VAMP8 as a novel regulator of the IFN-I

25 The antibody response against WNV correlated well with the protection of vaccinated mi

26 for promoting an antiviral response against WNV infection; however, it is unclear how heterogeneity

27 of an IFN-induced antiviral response against WNV.

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

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

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

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

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

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

34 echnique for single-cell transcriptomics and WNV RNA detection.

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

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

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

38 Dissecting the interactions between WNV and host defenses both informs basic molecular virol

39 ral and the EJC protein RBM8A directly binds WNV RNA.

40 y activation of antiviral programs can block WNV infection.

41 neutralizing antibody repertoire elicited by WNV infection for potential therapeutic application, we

42 hat in TRIM6 knockout (TRIM6-KO) A549 cells, WNV replication is significantly increased and IFN-I ind

43 ly an analytical workflow to a comprehensive WNV genome collection to test the impact of environmenta

44 ereby WNV infection of human DCs compromises WNV-specific T cell immunity.

45 are no approved treatment options to control WNV infection.

46 ersifying the resources available to control WNV.

47 mortality after WNV infection and decreased WNV-specific IgG and neutralizing Ab responses.

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

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

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

51 WNV containing a NS1 deletion (WNV-DeltaNS1) could be efficiently trans complemented in

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

53 dulation profiles were associated with DENV, WNV and ZIKV infections.

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

55 inding indicates the potential of developing WNV-DeltaNS1 as a noninfectious vaccine.

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

57 e spatial and temporal components that drive WNV transmission.

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

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

60 n processing were not enriched in DCs during WNV infection.

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

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

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

64 ted neurons and presynaptic terminals during WNV neuroinvasive disease.

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

66 Efficient WNV clearance and moderate susceptibility to WNV-mediate

67 gnaling that was not activated during either WNV or Zika virus (ZIKV) infection.

68 gnaling that was not activated during either WNV or ZIKV infection.

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

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

71 y direction kernel is the best kernel to fit WNV human case data, supporting the hypothesis of long-r

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

73 ection against synapse elimination following WNV infection and decreased neuronal apoptosis with syna

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

75 underlying cellular heterogeneity following WNV infection for the development of targeted therapeuti

76 interferon-stimulated genes (ISGs) following WNV infection or IFN-beta treatment.

77 Surveillance for WNV primarily focuses on a measure of infection prevalen

78 c targets and develop effective vaccines for WNV infections.

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

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

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

82 eutic application, we isolated ten mAbs from WNV-infected individuals.

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

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

85 e show that in mice that have recovered from WNV or ZIKV infection, T cell-derived interferon-gamma (

86 itive impairment in patients recovering from WNV neuroinvasive disease.

87 Following recovery from WNV infection, mice showed presynaptic termini eliminati

88 Functionally, WNV-infected DCs dampened T cell activation and prolifer

89 Functionally, WNV-infected moDCs dampened allogenic CD4 and CD8 T cell

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

91 and Cx. quinquefasciatus exhibiting greater WNV divergence.

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

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

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

95 late to severe disease outcomes during human WNV infection.

96 and cognitive dysfunction that mirror human WNV neuroinvasive disease.

97 rsalis is the most important vector of human WNV infections in the region.

98 mosquito infection rates and reported human WNV cases.

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

100 rticles to PFU indicated that Slfn11 impairs WNV infectivity.

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

102 vel regulator of the IFN-I system.IMPORTANCE WNV is a mosquito-borne flavivirus that poses a threat t

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

104 IM6 in human cells results in an increase in WNV replication and alters the expression and function o

105 gain insight into host pathways involved in WNV infection, we performed a systematic affinity-tag pu

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

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

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

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

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

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

112 ld be used to better estimate uncertainty in WNV risk.

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

114 oth interact with WNV proteins and influence WNV infection.

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

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

117 her, our analysis provides new insights into WNV infection patterns in multiple hosts and highlights

118 ys post-infection protected mice from lethal WNV challenge.

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

120 cells is critical for protection from lethal WNV infection.

121 mAb WNV-86 neutralized WNV with a 50% inhibitory concentrati

122 Mechanistically, WNV and ZIKV actively blocked STAT5 phosphorylation down

123 Mechanistically, WNV and ZIKV showed differential inhibition of Jak kinas

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

125 Neuroinvasive WNV infection results in encephalitis and can lead to pr

126 mAb WNV-86 neutralized WNV with a 50% inhibitory concentration of 2 ng ml(-1),

127 KV), Japanese encephalitis (JEV), West Nile (WNV), and yellow fever (YFV) viruses by intracellular cy

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

129 defective West Nile virus (WNV) lacking NS1 (WNV-DeltaNS1) that could propagate at low levels (10(5)

130 e sought to better understand the ability of WNV to program human dendritic cells (DCs) to prime WNV-

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

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

133 Further, a rapid contraction of WNV-specific CD8+ T cells in the brain correlated with p

134 hage polarization in vivo and the control of WNV infection through potential downstream control of AT

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

136 ive Vero cells after continuous culturing of WNV-DeltaNS1 in Vero(NS1) cells for 15 rounds.

137 nding the long-range spatial distribution of WNV.

138 2, highlighting a high genetic diversity of WNV genotypes in our region.

139 Finally, a single dose of WNV-86 administered two days post-infection protected mi

140 Vaccination with a single dose of WNV-DeltaNS1 protected mice from a highly lethal challen

141 R(-/-) mice were administered a high dose of WNV-DeltaNS1.

142 We evaluated the safety and efficacy of WNV-DeltaNS1 in mice.

143 with disease and lines that remained free of WNV neuroinvasion and disease.

144 fically, Slfn11 decreases the infectivity of WNV potentially by preventing virus-induced modification

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

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

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

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

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

150 Mouse models of WNV infection demonstrate that a proinflammatory environ

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

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

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

154 real-time forecast of seasonal outbreaks of WNV.

155 159 of the E protein in the pathogenesis of WNV infection.

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

157 the E protein modulates the pathogenicity of WNV by affecting viral replication and T-cell infiltrati

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

159 human DC activation to compromise priming of WNV-specific T cell immunity.IMPORTANCE West Nile virus

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

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 TCRm staining of WNV-infected cells demonstrated that the immunorecessive

165 s, likely at the protein translation step of WNV replication.

166 lowing infection with a pathogenic strain of WNV.

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

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

169 demonstrated the feasibility and utility of WNV-inclusive scRNA-seq as a high-throughput technique f

170 1)) that significantly improved the yield of WNV-DeltaNS1 (10(8) IU/ml).

171 th much greater efficiency than does DENV or WNV.

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

173 mals were fully protected against pathogenic WNV infection.

174 Here, we present WNV-inclusive single-cell RNA sequencing (scRNA-seq), an

175 Intriguingly, Slfn11 prevented WNV-induced downregulation of a subset of tRNAs implicat

176 program human dendritic cells (DCs) to prime WNV-specific T cell responses.

177 ns of human dendritic cells (DCs) in priming WNV-specific T cell immunity remains poorly understood.

178 ata, supporting the hypothesis of long-range WNV transmission is mainly along the migratory bird flyw

179 We produced recombinant WNV with the structural proteins of the NY99 or Eg101 st

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

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

182 N-I pathway that are important in regulating WNV replication are incompletely defined.

183 ast to the induction of antiviral responses, WNV infection did not promote transcription or secretion

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

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

186 trongly correlate with development of severe WNV neuroinvasive disease.

187 Transmitted primarily by Culex species, WNV transmission requires the complex interplay between

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

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

190 to demonstrate a new technique for studying WNV infection at the single-cell level.

191 e effective in protecting against subsequent WNV infection in wt cells than TRIM6-KO, indicating that

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

193 We find that WNV lineages tend to disperse faster in areas with highe

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

195 We found that WNV, dengue and Zika virus capsids interact with a conse

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

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

198 RBM8A binding to viral RNA, suggesting that WNV sequesters PYM1 to protect viral RNA from decay.

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

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

201 ions between the different conformers of the WNV frameshift signal was maximal in the range of forces

202 rate additional networks and pathways of the WNV immune response that cannot be observed in the C57BL

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

204 y the ribosome during PRF, we found that the WNV frameshift signal formed an unusually large number o

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

206 No adverse effects related to the WNV-DeltaNS1 vaccination were observed.

207 In contrast to WNV, ZIKV inhibited JAK1 and TYK2 phosphorylation follow

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

209 r understanding of the antiviral response to WNV infection is mostly derived from analysis of bulk ce

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

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

212 of each RLR in the innate immune response to WNV.

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

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

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

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

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

218 Using WNV as a model, we developed a new vaccine platform for

219 West Nile virus (WNV) and Zika virus (ZIKV) infect human dendritic cells

220 s with dengue virus (DENV), West Nile virus (WNV) and Zika virus (ZIKV) usually present similar mild

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

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

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

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

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

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

227 West Nile virus (WNV) has become the most epidemiologically important mos

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

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

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

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

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

233 , and evaluated against the West Nile virus (WNV) infection.

234 y from Zika virus (ZIKV) or West Nile virus (WNV) infection.

235 West Nile Virus (WNV) infections continue to grow in the US.

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

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

238 rapeutic targets.IMPORTANCE West Nile virus (WNV) is a clinically relevant pathogen responsible for r

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

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

241 West Nile Virus (WNV) is a mosquito-borne infection that can cause seriou

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

243 West Nile virus (WNV) is a neurotropic flavivirus and the leading cause o

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

245 West Nile virus (WNV) is a neurotropic mosquito-borne flavivirus of globa

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

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

248 West Nile virus (WNV) is an emerging mosquito-borne flavivirus, related t

249 T cell immunity.IMPORTANCE West Nile virus (WNV) is an encephalitic flavivirus that remains endemic

250 West Nile virus (WNV) is an important cause of viral encephalitis in bird

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

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

253 ced a replication-defective West Nile virus (WNV) lacking NS1 (WNV-DeltaNS1) that could propagate at

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

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

256 ecovery from infection with West Nile virus (WNV) or Zika virus (ZIKV) impact hippocampal-dependent l

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

258 rate host's IFN-I response, West Nile virus (WNV) replication is sensitive to pretreatment with IFN-I

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

260 approach by focusing on the West Nile virus (WNV) spread in North America that has substantially impa

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

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

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

264 West Nile virus (WNV), a member of the Flavivirus genus, is a leading cau

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

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

267 (DENV), Zika virus (ZIKV), West Nile virus (WNV), and hepatitis C virus (HCV).

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

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

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

271 Postinfection with West Nile virus (WNV), BAFF increased in CD8(-) cDCs and Nphs, and BAFF(+

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

273 Flavivirus genus, including West Nile virus (WNV), dengue virus (DENV), and Zika virus (ZIKV), but ha

274 of flaviviruses, including West Nile virus (WNV), dengue virus (DENV), and Zika virus (ZIKV).

275 f CC-F1 lines infected with West Nile virus (WNV), including comprehensive immunophenotyping, to iden

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

277 the frameshift signal from West Nile virus (WNV), which stimulates -1 PRF at very high levels and ha

278 West Nile virus (WNV)-a mosquito-borne arbovirus-entered the USA through

279 V, dengue virus (DENV), and West Nile virus (WNV).

280 signaling or infection with West Nile virus (WNV).

281 (e.g., measles virus [MV], West Nile virus [WNV], Sindbis virus [SV], rabies virus [RV], and influen

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

283 Combined, our data support a model whereby WNV infection of human DCs compromises WNV-specific T ce

284 ese observations, we propose a model whereby WNV subverts human DC activation to compromise priming o

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

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

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

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

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

290 Consistent with WNV's sensitivity to IFN-I, we found that in TRIM6 knock

291 A single-dose immunization with WNV-DeltaNS1 elicited robust immune responses in mice.

292 vels of neurovirulence in mice infected with WNV NY99 or Eg101.

293 Infection with WNV results in febrile illness, which can progress to se

294 nterferon [IFN] signaling) or infection with WNV.

295 ng revealed 26 genes that both interact with WNV proteins and influence WNV infection.

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

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

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

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

300 mice from a highly lethal challenge with WT WNV.

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