ライフサイエンスコーパス: TMEV

1 TMEV infected female mice had significantly decreased op

2 TMEV infection led to significantly decreased mu, delta

3 TMEV infection of normally resistant B10 mice results in

4 TMEV infection of susceptible mice leads to a persistent

5 TMEV infection of susceptible PL/J mice deficient in CD4

6 TMEV largely persists in macrophages (Ms) in the CNS, an

7 TMEV-induced demyelinating disease (TMEV-IDD) is conside

8 TMEV-infected mice depleted of CD11b(+)Ly6C(+) cells dur

9 TMEV-infected mice depleted of CD11b(+)Ly6C(+) cells had

10 TMEV-infected mice develop a demyelinating disease with

11 TMEV-specific lymphoproliferative responses, interleukin

12 rrying an IL-6 transgene (IL-6 Tg) develop a TMEV-induced demyelinating disease accompanied by an inc

13 se was also observed in mice infected with a TMEV encoding PLP139-151 with an amino acid substitution

14 ximal expression of PDL-1 but not PD-1 after TMEV infection using IL-6-deficient mice and IL-6-transg

15 hose of control mice at 14 and 21 days after TMEV infection.

16 o upregulate PD-1 and PDL-1 expression after TMEV infection in vitro, indicating that type I IFN sign

17 Therefore, endogenous IL-6 expression after TMEV infection is dependent on ERK MAPK, enhanced by IL-

18 Three weeks after TMEV infection, axonal degeneration was induced in the p

19 erative responses or antibody titers against TMEV among the groups.

20 Although TMEV-IDD is initiated by virus-specific CD4(+) T cells t

21 Although TMEV-induced demyelinating disease (TMEV-IDD) is thought

22 lammation, virus antigen-positive cells, and TMEV-specific lymphoproliferative responses versus infec

23 n was measured in TMEV-susceptible SJL/J and TMEV-resistant B10.S macrophages during their infection

24 are resistant to both viral persistence and TMEV-induced demyelinating disease.

25 There was no correlation between anti-TMEV antibody titers and disease course.

26 The generation of the anti-TMEV CD8(+) T-cell response in the brain requires primin

27 poptosis represents a mechanism to attenuate TMEV yet promote macrophage-to-macrophage spread during

28 Because TMEV can use axons to disseminate in the brain, axonal d

29 ic pathway is of particular interest because TMEV persists in the central nervous system of mice, lar

30 nd loss of opiate analgesia observed in both TMEV mice and multiple sclerosis patients.

31 ic T cells since these cells could kill both TMEV-infected and uninfected syngeneic or semisyngenic c

32 shed CD8+ T cell clones that could kill both TMEV-infected and uninfected syngeneic targets, although

33 eterogeneous neurological outcomes caused by TMEV and identify new models of human neurological disea

34 f astrocytes and other CNS-resident cells by TMEV provides the early NF-kappaB-mediated signals that

35 ing persistent infection in the mouse CNS by TMEV.

36 mune) mechanisms of demyelination induced by TMEV as well as other viruses.

37 sted whether an autoreactive cell induced by TMEV infection mediated cytotoxicity by using a 5-h (51)

38 Myelin destruction is initiated by TMEV-specific CD4(+) T cells targeting persistently infe

39 s induced in RAW264.7 cells, BMM, and SPM by TMEV.

40 Because immunosuppression of chronically TMEV-infected mice has been shown to enhance myelin repa

41 odominant virus peptide VP2121-130 and clear TMEV infection.

42 IFN-g signaling pathways, they do not clear TMEV infection and develop prominent neurological defici

43 MEV-derived peptide, VP2121-130, and cleared TMEV from the CNS.

44 Despite the increased CNS TMEV levels in these P1-Tg mice, B6 P1-Tg mice developed

45 phages, exogenous IL-6 resulted in decreased TMEV replication, earlier activation of STAT1 and STAT3,

46 yelitis virus-induced demyelinating disease (TMEV-IDD) is a mouse model of chronic-progressive multip

47 TMEV-induced demyelinating disease (TMEV-IDD) is considered to be a highly relevant animal m

48 yelitis virus-induced demyelinating disease (TMEV-IDD) is dependent on the activation of T cells to e

49 Although TMEV-induced demyelinating disease (TMEV-IDD) is thought to be immune mediated, there is als

50 yelitis virus-induced demyelinating disease (TMEV-IDD), a well-established animal model of primary pr

51 yelitis virus-induced demyelinating disease (TMEV-IDD).

52 eiler's virus-induced demyelinating disease (TMEV-IDD).

53 ing the VP2121-130 peptide before and during TMEV infection, 99% of the VP2121-130-specific CD8+ T ce

54 signaling events leading to apoptosis during TMEV infection, we screened baby hamster kidney (BHK-21)

55 brain to the spinal cord white matter during TMEV infection.

56 ain the dramatic loss in virus yields during TMEV-induced apoptosis and attenuate the virus, enabling

57 with Fab antibodies did not exacerbate early TMEV infection.

58 Costimulatory blockade inhibited early TMEV-specific T-cell and antibody responses critical in

59 Neutralizing Ab to TGF-beta1 eliminated TMEV-induced IL-23 production and SMAD-3 activation in R

60 train of Theiler's murine encephalomyelitis (TMEV-DA) virus induces persistent demyelinating lesions

61 Infection with the PLP139-151-encoding TMEV led within 10-14 days to a rapid-onset paralytic de

62 ly, infection with PLP139-151 mimic encoding TMEV serves as an excellent model for molecular mimicry

63 es comparable to those of controls following TMEV infection, and therefore PMNs and NK cells do not s

64 antly fewer seizures than controls following TMEV infection, indicating monocytes/macrophages and res

65 ficantly fewer behavioral seizures following TMEV infection, whereas mice depleted of complement comp

66 ficantly fewer behavioral seizures following TMEV infection.

67 These data suggest that, following TMEV infection of muscle, SHP-1 promotes M1 differentiat

68 n the CNS is primarily upregulated following TMEV infection via type I IFN signaling and the maximal

69 ep toward building a comprehensive model for TMEV-induced demyelinating disease.

70 id regions recognized by CD4(+) T cells from TMEV-infected mice using an overlapping peptide library.

71 Spleen cells from TMEV-infected mice were stimulated with irradiated TMEV

72 c CD4(+) T cells, CNS mononuclear cells from TMEV-infected SJL mice endogenously process and present

73 Spleen cells from TMEV-infected SJL/J mice stimulated with antigen-present

74 ction of IL-6 could protect macrophages from TMEV infection.

75 Here, TMEV infection induced splenic T cell depletion, which w

76 virus (SAFV) and a related virus named human TMEV-like cardiovirus (HTCV).

77 We asked if TMEV infection of microglia activates their innate immun

78 In TMEV infection, only Wld mice were paralyzed and had inc

79 acrophages inhibited muscle calcification in TMEV-infected WT animals.

80 To investigate the role of CD1d in TMEV infection, we first infected CD1d-deficient mice (C

81 s engaged by these protective CD8 T cells in TMEV-resistant strains remains unknown.

82 opioid receptor mRNA expression decreased in TMEV mice, we examined whether opiate analgesia is also

83 but not Gata3, in T cells was detrimental in TMEV infection.

84 croglia was considerably higher (>4-fold) in TMEV-infected SJL mice than TMEV-infected B6 mice.

85 ogeneic T cells, were significantly lower in TMEV-infected SJL mice than in B6 mice.

86 Therefore, IL-6 expression was measured in TMEV-susceptible SJL/J and TMEV-resistant B10.S macropha

87 d hippocampal neuronal loss were observed in TMEV-infected FVB/D(b) mice, but not in wild-type FVB mi

88 vitro do not differ from these processes in TMEV-infected BHK-21 cells, which undergo necroptosis.

89 hages did not differ from those processes in TMEV-infected BHK-21 cells, which undergo necroptosis.

90 ber of chemokines (ligands and receptors) in TMEV-infected and mock-infected C57BL/6 mice both with a

91 ur data implicate three of these residues in TMEV-cell receptor attachment.

92 ied cell types may play an important role in TMEV subgroup-specific disease phenotypes.

93 cted NKT cells may play a protective role in TMEV-induced neurological disease by alteration of the c

94 damage, though damaged axons were visible in TMEV-infected cultures.

95 st that during the acute phase of infection, TMEV targets neural cells for apoptosis without directly

96 In contrast, RCA I injection into TMEV-infected mice induced lesions in the posterior funi

97 nfected mice were stimulated with irradiated TMEV antigen-presenting cells and used as effector cells

98 rovides a potential mechanism for modulating TMEV neurovirulence during persistence in the mouse cent

99 we demonstrate that the high-neurovirulence TMEV GDVII virus uses the glycosaminoglycan heparan sulf

100 ophages infected with the low-neurovirulence TMEV BeAn virus became apoptotic through the mitochondri

101 Low-neurovirulence TMEV result in a persistent central nervous system infec

102 te autoimmune demyelination, a nonpathogenic TMEV variant was engineered to encode a 30-mer peptide e

103 1, into the coding region of a nonpathogenic TMEV variant.

104 did not result in the conversion of normally TMEV-resistant C57BL/6 mice to a susceptible phenotype.

105 The ability of TMEV to persist in the mouse CNS has traditionally been

106 Although our results show that activation of TMEV-specific CD8(+) T cells occurs in the peripheral ly

107 atory molecules PD-1 and PDL-1 in the CNS of TMEV-infected SJL mice and B6 mice.

108 capsid epitopes, were detected in the CNS of TMEV-infected SJL mice, whereas only a minor population

109 , we analyzed the phenotypic consequences of TMEV infection in the Collaborative Cross (CC) mouse pop

110 xogenous IL-6 enhances macrophage control of TMEV infection through preemptive antiviral nitric oxide

111 ignificantly decreased in the spinal cord of TMEV mice could explain the increased nociception and lo

112 g the latter 135 days of a 6-month course of TMEV-induced disease in susceptible (PLJ) or resistant (

113 he most prominent role in the development of TMEV-induced demyelinating disease.

114 To examine the direct effects of TMEV infection on neural cells, myelinated explant cultu

115 esent all the predominant T cell epitopes of TMEV to virus-specific T cell hybridomas, clones, as wel

116 n contrast, male mice have a higher level of TMEV-specific CD4(+) and CD8(+) T cell infiltration into

117 Our results indicated that message levels of TMEV, tumor necrosis factor alpha, beta interferon, and

118 J mice induce significantly higher levels of TMEV-specific neutralizing Ab as well as a stronger peri

119 e essential to investigate the mechanisms of TMEV-induced inflammation in the CNS of SHP-1-deficient

120 D80, and CD86) is higher on the microglia of TMEV-resistant C57BL/6 (B6) mice than the microglia of T

121 tant C57BL/6 (B6) mice than the microglia of TMEV-susceptible SJL/J (SJL) mice.

122 constructed the first mathematical model of TMEV-host kinetics during acute and early chronic infect

123 In the light of the known neurotropism of TMEV and the new human SAFV-1 and SAFV-2, the resulting

124 resent study, we analyzed the copy number of TMEV genomes, plus- to minus-strand ratios, and full-len

125 hages and significantly delayed the onset of TMEV-induced paralysis.

126 ays an important role in the pathogenesis of TMEV-IDD.

127 kine gene activation and the pathogenesis of TMEV-induced demyelinating disease are largely unknown.

128 e cerebellum were infected with 10(5) pfu of TMEV-DA for periods ranging from 1 to 72 h.

129 ning resveratrol during the chronic phase of TMEV-IDD.

130 5 plays a critical role in the production of TMEV-induced alpha interferon (IFN-alpha) during early v

131 ypothesis that virus capsid gene products of TMEV stimulate class I-restricted CD8(+) T-cell immune r

132 cts on the severity of the clinical signs of TMEV-induced disease in male and female mice.

133 fined CTL epitope shared by the DA strain of TMEV and other closely related cardioviruses.

134 In contrast, the GDVII strain of TMEV causes acute lethal encephalitis with no virus pers

135 on of susceptible mice with the DA strain of TMEV results in an acute polioencephalomyelitis followed

136 leader protein region of the BeAn strain of TMEV.

137 te the pathogenic mechanisms, two strains of TMEV (DA and BeAn), capable of inducing chronic demyelin

138 nt after infection with these two strains of TMEV and may differentially influence the pathogenic and

139 Certain strains of TMEV may cause a chronic demyelinating disease, which is

140 Other strains of TMEV only cause an acute infection without persistence i

141 elitis, treatment of SJL mice at the time of TMEV infection with murine CTLA-4 immunoglobulin or a co

142 mice undergoing PLP178-191-induced R-EAE or TMEV-IDD occurs directly in the CNS and not in the cervi

143 Other TMEV strains and mutants (GDVII, WW, BeAn 8386 [BeAn], D

144 complex structure of DA virus, a persistent TMEV, and the receptor moiety mimic, sialyllactose, refi

145 is a receptor moiety only for the persistent TMEV strains and not for the nonpersistent strains.

146 sed in FVB-D(b) mice resistant to persistent TMEV infection.

147 PLP139-TMEV-infected mice developed a rapid onset paralytic inf

148 nset demyelinating disease induced by PLP139-TMEV is the direct result of autoreactive PLP139-151-spe

149 P139-151-specific CD4(+) T cells from PLP139-TMEV-infected mice transferred demyelinating disease to

150 al disease symptoms in mice with preexisting TMEV-IDD.

151 us times after infection, virus replication, TMEV antigen expression, and demyelination were monitore

152 se toward the immunodominant D(b)-restricted TMEV-derived peptide, VP2121-130, and cleared TMEV from

153 -Tg mice developed significantly less severe TMEV-induced demyelinating disease.

154 veratrol developed significantly more severe TMEV-IDD than the control group.

155 Most significantly, TMEV-infected microglia were able to efficiently process

156 As such, TMEV-induced demyelinating disease in mice provides a hi

157 her (>4-fold) in TMEV-infected SJL mice than TMEV-infected B6 mice.

158 In this study, we demonstrated that TMEV RNA isolated from the spinal cords of chronically i

159 This is the first report demonstrating that TMEV can induce autoreactive cytotoxic cells that induce

160 We find that TMEV-induced cytokine gene expression is mediated by the

161 Our results indicate that TMEV-DA replicates in cultured neural tissue.

162 Our results indicated that TMEV infection induces the expression of both PD-1 and P

163 numbers steadily increased, indicating that TMEV persistence involves active viral RNA replication.

164 of infectivity assays led to the notion that TMEV persists at low levels.

165 These results suggest that TMEV persistence requires active viral replication begin

166 The TMEV L protein has been identified as important in the p

167 The TMEV-induced autoreactive cells were also different from

168 , and VP3] mapping to the left of VP1 in the TMEV genome) developed virus persistence and subsequent

169 fic T cells that migrate to the brain in the TMEV model has not been defined.

170 The site of antigenic challenge in the TMEV model is directly into the brain parenchyma, a site

171 we determined the gender differences in the TMEV-specific immune response, which may be responsible

172 ion by reducing microglial activation in the TMEV.

173 nsgenic mice expressing the P1 region of the TMEV genome (P1-Tg) were employed.

174 quent clinical disease in the context of the TMEV infection and not when administered in complete Fre

175 Thus, TMEV infection of microglia activates these cells to ini

176 (I:C), which is an innate immune agonist, to TMEV-infected mice during the innate immune response res

177 istration of IFN-beta, but not IFN-alpha, to TMEV- infected mice led to reduced myelin-specific CD4(+

178 thogenic CD4(+) T-cell responses directed to TMEV appear to be epitope dependent, and the differences

179 ypes of genomic regions previously linked to TMEV susceptibility to test the hypothesis that genomic

180 restricted response may confer resistance to TMEV-induced demyelinating disease, which is known to be

181 Although C57BL/6 mice normally resistant to TMEV infection with viral clearance, we have previously

182 to Salmonella and the other was resistant to TMEV.

183 e pGL3 promoter-reporter vector responded to TMEV or poly(I:C), a TLR3 agonist in the RAW264.7 macrop

184 n expression in RAW264.7 cells responding to TMEV.

185 and function of CTL generated in response to TMEV infection, we generated a panel of overlapping 20-m

186 the possibility that the immune response to TMEV is initiated by a brain-resident, bone marrow-deriv

187 I IFNs during the innate immune response to TMEV.

188 V) infection, expressed IL-23 in response to TMEV.

189 n variable disease phenotypes in response to TMEV.

190 ferent levels of intrinsic susceptibility to TMEV infection, cytokine production, and T-cell activati

191 viral immunity and confers susceptibility to TMEV infection.

192 tical for the differential susceptibility to TMEV-induced demyelinating disease between SJL and B6 mi

193 expression in T cells, became susceptible to TMEV infection with viral persistence.

194 esently known theiloviruses into five types: TMEV, VHEV, TRV, SAFV-1, and SAFV-2.

195 modeling has not been used for understanding TMEV infection.

196 serve as an important tool in understanding TMEV infectious mechanisms and may prove useful in evalu

197 Unlike TMEV and encephalomyocarditis virus, each of which is mo

198 eld of virology, especially to those who use TMEV as a murine model for multiple sclerosis.

199 erefore, we used BeAn virus, a less virulent TMEV, to study the effect of site-specific mutation of s

200 tion of Theiler's murine encephalitis virus (TMEV), a picornavirus from which it was derived.

201 cluding Theiler's murine encephalitis virus (TMEV), vesicular stomatitis virus (VSV), Sindbis virus,

202 th Theiler's murine encephalomyelitis virus (TMEV) and in mice with experimental autoimmune encephalo

203 s: Theiler's murine encephalomyelitis virus (TMEV) and myelin oligodendrocyte glycoprotein (MOG)-indu

204 to Theiler's murine encephalomyelitis virus (TMEV) because the GDVII strain and members of the GDVII

205 Theiler's murine encephalomyelitis virus (TMEV) belongs to the family Picornaviridae and causes de

206 ch Theiler's murine encephalomyelitis virus (TMEV) binds and enters host cells and the molecules invo

207 Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease in infected mice wh

208 of Theiler's murine encephalomyelitis virus (TMEV) causes a persistent central nervous system (CNS) i

209 of Theiler's murine encephalomyelitis virus (TMEV) causes an acute fatal polioencephalomyelitis in mi

210 th Theiler's murine encephalomyelitis virus (TMEV) cleared virus infection from anterior horn cell ne

211 he Theiler's murine encephalomyelitis virus (TMEV) compared to infected wild-type mice.

212 of Theiler's murine encephalomyelitis virus (TMEV) engineered to express a naturally occurring Haemop

213 nd Theiler's murine encephalomyelitis virus (TMEV) in MHC-congenic mouse strains where one haplotype

214 th Theiler's murine encephalomyelitis virus (TMEV) in the central nervous system (CNS) causes an immu

215 th Theiler's murine encephalomyelitis virus (TMEV) in the central nervous system (CNS) of susceptible

216 of Theiler's murine encephalomyelitis virus (TMEV) induce a persistent central nervous system infecti

217 of Theiler's murine encephalomyelitis virus (TMEV) induce an early transient subclinical neuronal dis

218 th Theiler's murine encephalomyelitis virus (TMEV) induces an immune-mediated demyelinating disease i

219 of Theiler's murine encephalomyelitis virus (TMEV) induces demyelination and a neurological disease i

220 th Theiler's murine encephalomyelitis virus (TMEV) induces immune-mediated demyelinating disease in s

221 Theiler's murine encephalomyelitis virus (TMEV) induces two distinct cell death programs, necrosis

222 th Theiler's murine encephalomyelitis virus (TMEV) induces various cytokines via Toll-like receptor-

223 he Theiler's murine encephalomyelitis virus (TMEV) infection and mouse hepatitis virus (MHV) infectio

224 on Theiler's murine encephalomyelitis virus (TMEV) infection and potential mechanisms in order to del

225 al Theiler's murine encephalomyelitis virus (TMEV) infection in mice induces inflammatory demyelinati

226 Theiler's murine encephalomyelitis virus (TMEV) infection in mice results in establishment of viru

227 Theiler's murine encephalomyelitis virus (TMEV) infection induces immune-mediated demyelinating di

228 Theiler murine encephalomyelitis virus (TMEV) infection of a mouse's central nervous system is b

229 ng Theiler's murine encephalomyelitis virus (TMEV) infection of macrophages, it is thought that high

230 Theiler's murine encephalomyelitis virus (TMEV) infection of SJL/J mice causes persistent infectio

231 at Theiler's murine encephalomyelitis virus (TMEV) infection of skeletal myofibers induces inflammati

232 Theiler's murine encephalomyelitis virus (TMEV) infection of the brain induces a virus-specific CD

233 In Theiler's murine encephalomyelitis virus (TMEV) infection, an animal model for multiple sclerosis

234 nd Theiler's murine encephalomyelitis virus (TMEV) infection.

235 by Theiler's murine encephalomyelitis virus (TMEV) infection.

236 ng Theiler's murine encephalomyelitis virus (TMEV) infection.

237 Theiler's murine encephalomyelitis virus (TMEV) is a highly cytolytic picornavirus that persists i

238 by Theiler's murine encephalomyelitis virus (TMEV) is a model for neurological outcomes caused by vir

239 Theiler's murine encephalomyelitis virus (TMEV) is a natural mouse pathogen which causes a lifelon

240 Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus of the Cardiovirus genus.

241 Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups based on neurovirule

242 us Theiler's murine encephalomyelitis virus (TMEV) leads to a progressive CD4(+) T cell-mediated demy

243 he Theiler's murine encephalomyelitis virus (TMEV) model of MS to examine possible changes in spinal

244 he Theiler's murine encephalomyelitis virus (TMEV) model of multiple sclerosis (MS).

245 he Theiler's murine encephalomyelitis virus (TMEV) model of multiple sclerosis, an effective central

246 of Theiler's murine encephalomyelitis virus (TMEV) persistently infects cells of the spinal cord duri

247 Theiler's murine encephalomyelitis virus (TMEV) persists in the mouse central nervous system princ

248 of Theiler's murine encephalomyelitis virus (TMEV) produce a chronic demyelinating disease in which t

249 of Theiler's murine encephalomyelitis virus (TMEV) resulted in acute behavioral seizures in approxima

250 Theiler's murine encephalomyelitis virus (TMEV) results in a persistent central nervous system inf

251 of Theiler's murine encephalomyelitis virus (TMEV) results in a persistent CNS infection, leading to

252 of Theiler's murine encephalomyelitis virus (TMEV) results in the production of an attenuated virus t

253 of Theiler's murine encephalomyelitis virus (TMEV) RNA replication in the central nervous systems of

254 ce Theiler's murine encephalomyelitis virus (TMEV) strain GDVII uses heparan sulfate (HS) as a corece

255 ee Theiler's murine encephalomyelitis virus (TMEV) strains (TO Yale, TOB15, and Vie 415HTR) and of Vi

256 he Theiler's murine encephalomyelitis virus (TMEV) subgroup of cardioviruses and is most closely rela

257 ed Theiler's murine encephalomyelitis virus (TMEV) to induce a chronic progressive CNS demyelinating

258 he Theiler's murine encephalomyelitis virus (TMEV) under the control of a class I major histocompatib

259 th Theiler's murine encephalomyelitis virus (TMEV) undergo apoptosis, resulting in restricted virus y

260 Theiler's murine encephalomyelitis virus (TMEV), a member of the Cardiovirus genus in the family P

261 of Theiler's murine encephalomyelitis virus (TMEV), a member of the Cardiovirus genus of the family P

262 Theiler's murine encephalomyelitis virus (TMEV), a natural pathogen of mice, is a member of the ge

263 th Theiler's murine encephalomyelitis virus (TMEV), a picornavirus that, in some strains of mice, res

264 ng Theiler's murine encephalomyelitis virus (TMEV), result in the vigorous production of IL-6.

265 th Theiler's murine encephalomyelitis virus (TMEV), the levels of mRNAs encoding chemokines MCP-1/CCL

266 Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease is a chronic-progres

267 Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease is a relevant mouse

268 he Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease model of multiple sc

269 Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease serves as a relevant

270 in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease, a viral model for m

271 s, Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease, also displays a gen

272 Theiler's murine encephalomyelitis virus (TMEV)-induced immune-mediated demyelinating disease in s

273 he Theiler's murine encephalomyelitis virus (TMEV)-induced seizure model.

274 in Theiler's murine encephalomyelitis virus (TMEV)-infected transgenic FVB mice that express the D(b)

275 th Theiler's murine encephalomyelitis virus (TMEV).

276 of Theiler's murine encephalomyelitis virus (TMEV).

277 om Theiler's murine encephalomyelitis virus (TMEV; BeAn) and Saffold virus interact similarly in any

278 elinating disease following Theiler's virus (TMEV) infection, expressed IL-23 in response to TMEV.

279 ., Theiler's murine encephalomyelitis virus [TMEV]) are members of the Picornaviridae family that cau

280 Theiler's murine encephalomyelitis viruses (TMEV) consist of two groups, the high- and low-neuroviru

281 Theiler's murine encephalomyelitis viruses (TMEV), such as BeAn virus, cause a persistent infection

282 Theiler's murine encephalomyelitis viruses (TMEV).

283 iceptive tests beginning at day 90 PI, while TMEV-infected male mice did not display significantly de

284 cells and SJL/J SPM following challenge with TMEV.

285 SJL/J mice were infected with TMEV and fed a control diet or a diet containing resvera

286 glia lines can be persistently infected with TMEV and that infection significantly upregulates the ex

287 Control mice, infected with TMEV but receiving no RCA I, had inflammatory demyelinat

288 Abeta(0).beta2m(0) mice infected with TMEV died within 18 days of infection.

289 Most significantly, mice infected with TMEV encoding a Haemophilus influenzae mimic peptide, sh

290 sidue (H147A), but not in mice infected with TMEV encoding a PLP139-151 substitution at the primary T

291 e induction in mice previously infected with TMEV led to a severe, often fatal reaction.

292 with antigen-presenting cells infected with TMEV resulted in a population of autoreactive CD8+ cytot

293 esions of SJL mice chronically infected with TMEV.

294 ice were cultured in vitro and infected with TMEV.

295 10.S macrophages during their infection with TMEV DA strain or responses to lipopolysaccharide (LPS)

296 Following intracerebral infection with TMEV, all three lines of mice survived the acute encepha

297 d in situ upon intracranial inoculation with TMEV.

298 we show that the infection of SJL mice with TMEV expressing the H. influenzae mimic can exacerbate a

299 The infection of susceptible mice with TMEV induces the development of chronic demyelinating di

300 during the first 24 h after stimulation with TMEV, LPS, or poly(I . C).