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

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

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

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

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

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

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

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

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

34 ing persistent infection in the mouse CNS by TMEV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 with Fab antibodies did not exacerbate early TMEV infection.

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

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

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

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

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

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

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

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

65 ficantly fewer behavioral seizures following TMEV infection.

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

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

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

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

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

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

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

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

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

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

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

77 ng of CD8 T cells against the immunodominant TMEV peptide VP2(121-130) Loss of H-2D(b) on CD11c(+) AP

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 We show that 2A is also required for PRF in TMEV and can stimulate PRF to levels as high as 58% in r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 5 plays a critical role in the production of TMEV-induced alpha interferon (IFN-alpha) during early v

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

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

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

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

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

135 (I.C.) injection of Daniel's (DA) strain of TMEV, there is vigorous immune response, which is detrim

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 We also show that TMEV 2A trans-activates PRF on the EMCV signal but not v

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 e antiviral CD8 T cell responses against the TMEV immunodominant epitope VP2(121-130), with functiona

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

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

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

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

173 ion by reducing microglial activation in the TMEV.

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

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

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

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

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

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

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

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

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

183 to Salmonella and the other was resistant to TMEV.

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

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

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

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

188 n variable disease phenotypes in response to TMEV.

189 I IFNs during the innate immune response to TMEV.

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

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

192 viral immunity and confers susceptibility to TMEV infection.

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

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

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

196 modeling has not been used for understanding TMEV infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 a well-characterized experimenta

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

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

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

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

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

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

234 Theiler's murine encephalomyelitis virus (TMEV) infection of the CNS is cleared in C57BL/6 mice by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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) RNA replication in the central nervous systems of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 ed 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).