ライフサイエンスコーパス: LCMV

1 LCMV infection induces a remarkable influx of inflammato

2 lymphocytic choriomeningitis virus clone 13 (LCMV cl13).

3 H(2)O(2)-LCMV vaccination protected animals against challenge wit

4 By day 38, LCMV-specific IgG ASC were decreased 5-fold in the bone

5 cell response, and to predict and generate a LCMV cross-reactive response toward a variant of a null

6 stimulation were reduced 8 days after acute LCMV infection but recovered to preinfection levels by 6

7 d compared them to those induced by an acute LCMV infection.

8 However, during acute LCMV infection, neither systemic cytokine patterns nor t

9 imal antiviral T cell responses during acute LCMV infection.

10 inal lymph nodes (mLNs) throughout the acute LCMV response of IAV-immune mice.

11 memory phase of the immune response to acute LCMV infection.

12 e MCMV persistently infected mice with acute LCMV infection (7 of 36) developed a robust immunodomina

13 However, Treg cell numbers collapsed after LCMV inoculation.

14 bserved that anti-OX40 injection early after LCMV clone 13 infection increased CD8 T cell-mediated im

15 monocytes outnumber Kupffer cells 24 h after LCMV infection, it is highly likely that inflammatory mo

16 able as APCs for protective immunity against LCMV infection.

17 e was reached, latently infected mice had an LCMV-specific memory T cell pool that was increased rela

18 Further, germinal center formation and LCMV-specific Ab responses were not impaired in DeltaDC

19 nses, which cross-reacted with LCMV-GP34 and LCMV-GP276, respectively.

20 rus, which is a genetic relative of LASV and LCMV-Arm induced robust responses that were TLR2/Mal dep

21 atory cells but was also detected on Th1 and LCMV-specific CD8 T cells at day 8 p.i. and was maintain

22 -yl]ethanamide), which exhibited strong anti-LCMV activity in the absence of cell toxicity.

23 sponse to ex vivo stimulation with antigenic LCMV peptides, although IL-7R expression was reduced in

24 binant versions of the prototypic arenavirus LCMV encoding codon-deoptimized viral nucleoproteins (rL

25 Here we have used the prototypic arenavirus LCMV to document a general molecular strategy for arenav

26 ckade of PKR function is highly specific, as LCMV is unable to similarly inhibit eIF2alpha phosphoryl

27 has been studied mostly with viruses such as LCMV that are cleared, but the situation can be more com

28 crystal structures of K(b)-VV-A11R and K(b)-LCMV-gp34.

29 ifferences in neither viral kinetics between LCMV infections of Axl(-/-) and wild-type mice nor T-cel

30 ated oncolytic viruses and to PD-1 blockade, LCMV treatment shows promising antitumoural benefits.

31 Both LCMV and PVM infections resulted in reduced osteoblast-s

32 us-reactive T cell responses in vivo to both LCMV and influenza virus infections.

33 interferon gamma than CD4 T cells induced by LCMV infection.

34 ecreased Th1 responses than those induced by LCMV infection.

35 the endosome compartment that is mediated by LCMV glycoprotein GP2 and required to release the virus

36 Upon secondary challenge, LCMV-specific secondary effector CD8(+) T cells expanded

37 to decrease Treg cell levels, did not change LCMV titers but resulted in a surprising decrease in lun

38 o RNA viruses: lymphocytic choriomeningitis (LCMV) and influenza (Flu).

39 e well-studied lymphocytic choriomeningitis (LCMV) and Pichinde (PICV) viruses, several differences w

40 Chronic LCMV infection rapidly attenuates IFN-I responses, but e

41 ferentiation in the early phase of a chronic LCMV infection without inheriting a net survival or expa

42 T cells resembled stem cells during chronic LCMV infection, undergoing self-renewal and also differe

43 nd sustained IL-10 expression during chronic LCMV infection.

44 expressing human CD20, we found that chronic LCMV infection impaired the depletion of B cells with ri

45 ected animals against challenge with chronic LCMV clone 13, and protection was mediated by CD8(+) T c

46 gene 3) increased the number of circulating LCMV-specific CD8(+) T cells, and improved CD8(+) T cell

47 Importantly, ceramide-conditioned, LCMV-infected DCs displayed an increased ability to prom

48 In contrast, LCMV-injected Ins2-GP(Tg) mice lacking the p75NTR retain

49 In contrast, LCMV-specific effector CD4(+) T cells were increased in

50 es of IFNbeta versus IFNalpha in controlling LCMV infection.

51 y inflammatory macrophages and downmodulated LCMV-specific T-cell responses by limiting hyperactivati

52 or, and central memory CD8(+) T cells during LCMV infection.

53 learance and enhanced immunopathology during LCMV infection.

54 specific CD4 T cells compared to that during LCMV infection.

55 T cells while limiting expansion of effector LCMV-specific T cells.

56 otein (GP), followed by boosting with either LCMV Armstrong, which is rapidly controlled, or LCMV CL-

57 ansion and cytokine expression of endogenous LCMV-specific T cells was comparable between wild-type a

58 ce immunization with a DNA vector expressing LCMV-GP generated efficient CD4 Th1 responses.

59 ter immunization with Ad5 vectors expressing LCMV-GP in mice.

60 the crucial antiviral effector function for LCMV control was normal.

61 lls into primary CD8(+) T cells specific for LCMV GP(33-41) was relatively normal.

62 Restimulation of Th1 cells from LCMV-infected mice promoted BLIMP-1 and subsequent IL-10

63 id cells 2 (Trem2 (-/-)) were protected from LCMV-induced hepatitis and showed improved virus control

64 Further, LCMV coinfection of IFN-gamma-deficient mice promoted pa

65 duction in both the frequency of IFNgamma(+) LCMV-specific CD8(+) and CD4(+) T cells and the magnitud

66 Importantly, LCMV-specific memory CD8(+) T cells had decreased CD27 a

67 chondrial apoptosis remained fully active in LCMV-infected cells.

68 s-induced apoptosis remained fully active in LCMV-infected cells.

69 I independence of mitochondrial apoptosis in LCMV-infected cells provides the first evidence that are

70 Primary virus-specific CD8(+) T cells in LCMV clone-13-infected septic mice displayed exacerbated

71 emonstrate that the deletion of N-glycans in LCMV GP may confer an advantage to the virus for infecti

72 d T cell function and reduced viral loads in LCMV-infected animals.

73 Notably, in LCMV-infected cells, RIG-I was dispensable for virus-ind

74 The collapse of Treg cell numbers in LCMV-triggered perforin-deficient, but not wild-type, mi

75 tory phenotype with impaired phagocytosis in LCMV-induced liver inflammation but exhibit increased en

76 cific CD8 T cells was drastically reduced in LCMV-infected mice exposed to IAP antagonists.

77 xpression of IL-33 and ST2 is upregulated in LCMV-infected Prf1(-/-) mice.

78 O(2)-inactivated whole-virus vaccine induces LCMV-specific CD8(+) T cells with unique functional char

79 action studies revealed that F3406 inhibited LCMV cell entry by specifically interfering with the pH-

80 nt to treat myocardial infarction, inhibited LCMV propagation in culture cells.

81 Isotype switching and the initial LCMV-specific IgG response were normal in IL-21R(-/-) mi

82 al in persistently infected mice that lacked LCMV-specific antibodies.

83 mice infected with a variant strain of LCMV (LCMV V35A) bearing a mutation in the cognate major histo

84 ttenuated in vivo in a mouse model of lethal LCMV infection, but immunization with rLCMV/TransS confe

85 esponses were not impaired during Listeria + LCMV coinfection, arguing against a major role for this

86 odons in mammalian cells, which caused lower LCMV NP expression levels in transfected cells that corr

87 immune to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology, enhanc

88 When MCMV infection was given first (MCMV+LCMV), the magnitude of the acute T cell response to LCM

89 Mechanistically, LCMV induces antitumour immunity, which depends on the r

90 ry at 65 d post infection revealed many more LCMV-specific WT memory T cells than NIK KO memory T cel

91 virus (LCMV)-infected iFRCs activated naive LCMV-specific CD4(+) and CD8(+) T cells while limiting e

92 mulation was dispensable for accumulation of LCMV-specific CD8(+) T cells because of redundancy with

93 st that there is a risk of the appearance of LCMV acute encephalitis cases.

94 The Armstrong strain (ARM) of LCMV causes an acute infection, whereas its derivative,

95 Comparison of the characteristics of LCMV infection-induced HLH in the murine counterparts of

96 V infection but not the long-term control of LCMV infection.

97 HE activity contributed to the life cycle of LCMV remain unknown.

98 We report the first detection of LCMV RNA in a common European house mouse (Mus musculus

99 s led to altered effector differentiation of LCMV GP-specific CD4 T cells compared to that during LCM

100 genetic studies revealed that cell entry of LCMV in A549 cells depended on actin remodeling and Pak1

101 extent RNA synthesis, but not cell entry, of LCMV.

102 d an unexpected partial clonal exhaustion of LCMV-specific CD8(+) T-cell responses only in IAV-immune

103 ed with reduced numbers and functionality of LCMV-specific CD4(+) helper T cells and impaired antivir

104 We found that the history of LCMV infection intensifies MCMV immunopathology, enhance

105 resulted in a T-cell-intrinsic impairment of LCMV-specific Th1 effector responses in both mixed bone

106 de (EIPA) resulted in a robust inhibition of LCMV multiplication in both rodent (BHK-21) and human (A

107 put screen to rapidly identify inhibitors of LCMV multiplication.

108 l depletion, therapeutic antibody-killing of LCMV infected cells and human CD20-expressing tumors, as

109 using the well-characterized mouse model of LCMV infection revealed that rLCMV/NP(CD1) and rLCMV/NP(

110 as required for efficient multiplication of LCMV in HeLa cells, but the mechanisms by which NHE acti

111 1 p.i. increased the frequency and number of LCMV-specific CD8 T cells, resulting in increased in viv

112 Although the number of LCMV-specific effector CD8(+) T cells was not altered, t

113 logy was associated with a reduced number of LCMV-specific effector memory CD8 T cells.

114 ant treatment had no effect on the number of LCMV-specific IgG memory B cells.

115 V infection initially reduced the numbers of LCMV-specific memory T cells, but continued MCMV persist

116 The initial replication of LCMV was lower in latently infected mice, and the matura

117 n deleterious consequences in the setting of LCMV infection.

118 virus titres in the spleen and the spread of LCMV to peripheral organs.

119 bove baseline levels at the chronic stage of LCMV infection.

120 into mice infected with a variant strain of LCMV (LCMV V35A) bearing a mutation in the cognate major

121 3 (Cl-13) variant of the Armstrong strain of LCMV (rCl-13/LASV-GPC) exhibited Cl-13-like growth prope

122 after challenge with a persistent strain of LCMV.

123 cell interactions evolved through studies of LCMV in its natural murine host.

124 lockade of ST2 markedly improves survival of LCMV-infected Prf1(-/-) mice and reduces the severity of

125 also significantly improved the survival of LCMV-infectedPrf1(--)mice.

126 +) T cells were highly diverse, but those of LCMV D(b)/GP33-specific CTL, especially from KO mice, we

127 cytokine patterns nor the impact of Il10 on LCMV-induced immunopathology differed conspicuously betw

128 The alleviating effect of Il10 on LCMV-induced immunopathology was found to be operative i

129 ses emerged, in large part, from research on LCMV.

130 V Armstrong, which is rapidly controlled, or LCMV CL-13, which leads to a more prolonged exposure to

131 Peripheral LCMV infection can lead to rapid cytolytic clearance or

132 Upon viral challenge, persistent LCMV efficiently blocked induction of interferons, where

133 L-27R was critical for control of persistent LCMV in vivo.

134 h an agonist Ab had the potential to prevent LCMV persistence.

135 overabundant interferon (IFN)gamma-producing LCMV-specific CD8(+) T cells thought to arise from exces

136 Thus, Axl is not required for productive LCMV infection of mice.

137 sed reverse genetics to rescue a recombinant LCMV (rLCMV) containing a translocated viral S segment (

138 We have documented that a recombinant LCMV containing the glycoprotein (GPC) gene of LASV with

139 first time, the generation of a recombinant LCMV where the viral protein products encoded by the S R

140 e S genome segment to generate a recombinant LCMV, rLCMV(IGR/S-S), that was highly attenuated in vivo

141 Here we describe a novel recombinant LCMV and its use to develop a cell-based assay suitable

142 al challenge with wild-type (WT) recombinant LCMV (rLCMV/WT).

143 Remarkably, LCMV coinfection of mice that had healed from L. guyanen

144 Remarkably, LCMV-induced, T cell-mediated hepatitis is not affected

145 ong strain, but the more rapidly replicating LCMV-WE induced T cell exhaustion and viral persistence.

146 RIP-LCMV islets express CXCL10 after isolation and maintain

147 s from either normal or CXCL10-deficient RIP-LCMV mice and transferred them under the kidney capsule

148 Combination therapy of diabetic RIP-LCMV and NOD mice with anti-CD3 and anti-CXCL10 antibodi

149 hem under the kidney capsule of diabetic RIP-LCMV mice.

150 ented type 1 diabetes (T1D) in the mouse Rip-LCMV T1D model.

151 une destruction of islet isografts using RIP-LCMV mice expressing a lymphocytic choriomeningitis viru

152 ence of larger numbers of cytokine-secreting LCMV-specific CD8(+) T cells in miR-31-deficent mice tha

153 ce, M57727-734, and the normally subdominant LCMV epitope L2062-2069, indicating a profound private s

154 epitope sequence and a normally subdominant LCMV epitope.

155 in response to different types of systemic (LCMV, L. monocytogenes) and/or localized (influenza viru

156 We found that LCMV does not induce apoptosis at any time during infect

157 We observed that LCMV-specific CD8 T cells from chronically infected mice

158 Our study reveals that LCMV infection efficiently suppresses induction of IFN-I

159 In this report, we show that LCMV-NP, as well as NPs encoded by representative member

160 However, the LCMV-specific secondary memory CD8(+) T cell pool was de

161 n the presence of cross-reactive memory, the LCMV-specific response was overstimulated and became par

162 expressing an immunodominant epitope of the LCMV glycoprotein (GP33) was greatly accelerated, augmen

163 Swapping of the LCMV Z NTD into the nonpathogenic Pichinde virus (PICV)

164 Assessment of the LCMV-specific memory at 65 d post infection revealed man

165 Our results show that the LCMV cross-reactive T cell response toward vaccinia viru

166 nant Pichinde virus system, we show that the LCMV Z N-terminal domain (NTD) mediates the inhibition o

167 ill sufficient to control infection with the LCMV Armstrong strain, but the more rapidly replicating

168 severity of HLH was not correlated with the LCMV load and not fully with differences in the intensit

169 These LCMV-specific CD8(+) T cells expressed the PD-1 inhibito

170 gative for diabetes antigen tetramers and to LCMV (lymphocytic choriomeningitis)-reactive CD8+ T cell

171 In contrast to LCMV infection, where balanced CD4 T helper 1 (Th1) and

172 If mice were previously immune to LCMV and then infected with MCMV (LCMV+MCMV), they had m

173 duction was measured in serum in response to LCMV challenge and characterized in vivo by using IFN-I

174 he magnitude of the acute T cell response to LCMV declined with age though this age-dependent decline

175 The immune response to LCMV is characterized by an extended survival of virus-s

176 not further erode memory T cells specific to LCMV.

177 oinoculated mice with a mixture of wild-type LCMV and genetically engineered CTL epitope-deficient mu

178 e, against a lethal challenge with wild-type LCMV.

179 a subsequent lethal challenge with wild-type LCMV.

180 on against a lethal challenge with wild-type LCMV.

181 ty against a lethal challenge with wild-type LCMV.

182 ty against a lethal challenge with wild-type LCMV.

183 on against a lethal challenge with wild-type LCMV.

184 lammatory monocytes dramatically change upon LCMV exposure and resemble those of Kupffer cells.

185 their steady-state endocytic functions upon LCMV infection.

186 a surprising decrease in lung pathology upon LCMV infection in IAV-immune but not in naive mice.

187 contributes to enhancing lung pathology upon LCMV infection of IAV-immune mice.

188 e modeled CD8 T cell responses using vaginal LCMV infection.

189 atically different in response to LPS versus LCMV infection.

190 viruses, lymphocytic choriomeningitis virus (LCMV) and Lassa, Junin, Machupo, Sabia, Guanarito, Chapa

191 thogens, lymphocytic choriomeningitis virus (LCMV) and murine cytomegalovirus (MCMV).

192 ted with lymphocytic choriomeningitis virus (LCMV) and secondary (noninherited) HLH in which C57BL/6

193 ion with lymphocytic choriomeningitis virus (LCMV) and that these CD4 T cells differentiated into T f

194 aviruses lymphocytic choriomeningitis virus (LCMV) and the clinically used Junin virus vaccine (Candi

195 enavirus lymphocytic choriomeningitis virus (LCMV) and the New World arenavirus Junin virus (JUNV) st

196 ter with lymphocytic choriomeningitis virus (LCMV) and then monitored the course of infection.

197 ted with lymphocytic choriomeningitis virus (LCMV) and treated with Mn(III)tetrakis(4-benzoic acid)po

198 ons with lymphocytic choriomeningitis virus (LCMV) and vaccinia virus, where the pathogens are cleare

199 viruses, lymphocytic choriomeningitis virus (LCMV) and vaccinia virus.

200 y, using lymphocytic choriomeningitis virus (LCMV) and Zika virus (ZIKV) in wild-type mice, we show t

201 Using lymphocytic choriomeningitis virus (LCMV) as a model of a persistent virus infection and dra

202 how that lymphocytic choriomeningitis virus (LCMV) can also inhibit macrophage activation, in contras

203 Lymphocytic choriomeningitis virus (LCMV) can cause acute fatal disease on all continents bu

204 y 2 post-lymphocytic choriomeningitis virus (LCMV) clone 13 infection, but is downregulated to below

205 ted with lymphocytic choriomeningitis virus (LCMV) clone 13 into recipient mice that had cleared an a

206 ion with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-31-deficent mice recovered from clin

207 t virus, lymphocytic choriomeningitis virus (LCMV) clone 13, on early innate intrahepatic immune resp

208 ted with lymphocytic choriomeningitis virus (LCMV) clone 13, which is used as a model of persistent v

209 Lymphocytic choriomeningitis virus (LCMV) clone 13, which normally establishes a chronic inf

210 tible to lymphocytic choriomeningitis virus (LCMV) clone-13 infection exhibited by mortality and vira

211 ted with lymphocytic choriomeningitis virus (LCMV) exhibit a severe defect in Fcgamma-receptor (Fcgam

212 ted with lymphocytic choriomeningitis virus (LCMV) exhibit global perturbations of circulating serum

213 encoding lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP) and examined GP-specific CD4 T c

214 sing the lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP), followed by boosting with eithe

215 pressing lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP).

216 nding to lymphocytic choriomeningitis virus (LCMV) identified multiple genes that regulated developme

217 with the lymphocytic choriomeningitis virus (LCMV) in mice is significantly further increased in Il10

218 mans and lymphocytic choriomeningitis virus (LCMV) in mice.

219 otein of lymphocytic choriomeningitis virus (LCMV) in vitro.

220 bsequent lymphocytic choriomeningitis virus (LCMV) infection and can result in severe lung pathology,

221 chronic lymphocytic choriomeningitis virus (LCMV) infection and suppressed CTL survival and function

222 y during lymphocytic choriomeningitis virus (LCMV) infection by pharmacological targeting with an IAP

223 chronic lymphocytic choriomeningitis virus (LCMV) infection in an IL-10 reporter mouse line.

224 rsistent lymphocytic choriomeningitis virus (LCMV) infection in mice through suppression of virus-spe

225 chronic lymphocytic choriomeningitis virus (LCMV) infection models, we determined that pDCs transien

226 to acute lymphocytic choriomeningitis virus (LCMV) infection was predominantly D(b)/GP33 specific and

227 chronic lymphocytic choriomeningitis virus (LCMV) infection, before severe dysfunction develops, vir

228 nce of a lymphocytic choriomeningitis virus (LCMV) infection, but the virus can present a number of u

229 rsistent lymphocytic choriomeningitis virus (LCMV) infection, IFNalpha and IFNbeta are highly induced

230 ization, lymphocytic choriomeningitis virus (LCMV) infection, or herpes simplex virus 1 (HSV1) infect

231 o during lymphocytic choriomeningitis virus (LCMV) infection.

232 ty after lymphocytic choriomeningitis virus (LCMV) infection.

233 chronic lymphocytic choriomeningitis virus (LCMV) infection.

234 chronic lymphocytic choriomeningitis virus (LCMV) infection.

235 chronic lymphocytic choriomeningitis virus (LCMV) infection.

236 chronic lymphocytic choriomeningitis virus (LCMV) infection.

237 LH after lymphocytic choriomeningitis virus (LCMV) infection.

238 enavirus lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen of clinical signific

239 enavirus lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen of clinical signific

240 enavirus lymphocytic choriomeningitis virus (LCMV) is an important neglected human pathogen.

241 rains of lymphocytic choriomeningitis virus (LCMV) led to two distinct phases of innate immune respon

242 ted with lymphocytic choriomeningitis virus (LCMV) lost islet sympathetic nerves before diabetes deve

243 train of lymphocytic choriomeningitis virus (LCMV) or influenza virus.

244 h either lymphocytic choriomeningitis virus (LCMV) or pneumonia virus of mice (PVM) resulted in rapid

245 athogens lymphocytic choriomeningitis virus (LCMV) or vaccinia virus (VACV).

246 essing a lymphocytic choriomeningitis virus (LCMV) protein in the beta-cells.

247 ice with lymphocytic choriomeningitis virus (LCMV) results in massive expansion of virus-specific CD4

248 ion with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.

249 chronic lymphocytic choriomeningitis virus (LCMV) strains, we uncovered that T cell differentiation

250 ted with lymphocytic choriomeningitis virus (LCMV) suppressed multiple Fcgamma-receptor (FcgammaR) fu

251 The lymphocytic choriomeningitis virus (LCMV) system constitutes one of the most widely used mod

252 rth with lymphocytic choriomeningitis virus (LCMV) to demonstrate that therapeutic antiviral T cells

253 enavirus lymphocytic choriomeningitis virus (LCMV) to develop a general molecular strategy for arenav

254 enavirus lymphocytic choriomeningitis virus (LCMV) to interfere with RIG-I/MAVS-dependent apoptosis.

255 enavirus lymphocytic choriomeningitis virus (LCMV) to interfere with the induction of programmed cell

256 enavirus lymphocytic choriomeningitis virus (LCMV) with the least frequently used codons in mammalian

257 duced by lymphocytic choriomeningitis virus (LCMV), CD28/B7-mediated costimulation was dispensable fo

258 family, lymphocytic choriomeningitis virus (LCMV), disables the host innate defense by interfering w

259 ted with lymphocytic choriomeningitis virus (LCMV), disease is driven by overabundant interferon (IFN

260 navirus, lymphocytic choriomeningitis virus (LCMV), is a neglected human pathogen of clinical signifi

261 nsis and lymphocytic choriomeningitis virus (LCMV), or the sand fly-transmitted arbovirus Toscana vir

262 navirus, lymphocytic choriomeningitis virus (LCMV), provides investigators with a superb experimental

263 g virus, lymphocytic choriomeningitis virus (LCMV), rabies virus, and Lassa virus.

264 ged with lymphocytic choriomeningitis virus (LCMV), which we show in this study to have relatively mi

265 ronment, lymphocytic choriomeningitis virus (LCMV)-infected iFRCs activated naive LCMV-specific CD4(+

266 how that lymphocytic choriomeningitis virus (LCMV)-specific CD8+ T cells in nonlymphoid tissues were

267 spleens, lymphocytic choriomeningitis virus (LCMV)-specific T cell responses were not impaired during

268 chronic lymphocytic choriomeningitis virus (LCMV).

269 ice with lymphocytic choriomeningitis virus (LCMV).

270 enavirus lymphocytic choriomeningitis virus (LCMV).

271 ion with lymphocytic choriomeningitis virus (LCMV).

272 ion with lymphocytic choriomeningitis virus (LCMV).

273 e-strand lymphocytic choriomeningitis virus (LCMV).

274 train of lymphocytic choriomeningitis virus (LCMV).

275 such as lymphocytic choriomeningitis virus (LCMV).

276 enavirus lymphocytic choriomeningitis virus (LCMV).

277 ras with lymphocytic choriomeningitis virus (LCMV).

278 ion with lymphocytic choriomeningitis virus (LCMV).

279 ice with lymphocytic choriomeningitis virus (LCMV).

280 ncluding lymphocytic choriomeningitis virus (LCMV).

281 gered by lymphocytic choriomeningitis virus (LCMV).

282 ted with lymphocytic choriomeningitis virus (LCMV).

283 ion with lymphocytic choriomeningitis virus (LCMV).

284 VSV) and lymphocytic choriomeningitis virus (LCMV).

285 n of the lymphocytic choriomeningitis virus (LCMV-GP), creating a replicating therapeutic, rVSV(GP),

286 CMV) and lymphocytic choriomeningitis virus (LCMV; Cl13), in their natural rodent host, we observed t

287 viruses, including Ebola virus, Lassa virus, LCMV, rabies virus, and Marburg virus, which was substit

288 While LCMV efficiently blocked induction of IFN-I via RIG-I/MA

289 ytes limited osteoblast loss associated with LCMV infection.

290 e greater than those following boosting with LCMV Armstrong.

291 responses, during a high-dose challenge with LCMV clone 13, increased immunopathology was associated

292 hus, one might predict that coinfection with LCMV, which induces a strong systemic type 1 response, w

293 on model to study heterologous immunity with LCMV.

294 n by CD4 T lymphocytes during infection with LCMV cl13.

295 However, we found that infection with LCMV led to significantly enhanced disease in L. major-i

296 Although priming of naive mice with LCMV CL-13 normally results in T cell exhaustion and est

297 nflammation 24 h after inoculating mice with LCMV.

298 specific responses, which cross-reacted with LCMV-GP34 and LCMV-GP276, respectively.

299 ic memory CD8(+) T cells cross-reactive with LCMV.

300 mpared to those in mice infected solely with LCMV.