ライフサイエンスコーパス: LCMV

1 LCMV infection induces a remarkable influx of inflammato

2 LCMV infection is self-limited in wild-type mice, but Pr

3 LCMV-infected Il18-transgenic (Il18tg) mice developed ca

4 lymphocytic choriomeningitis virus clone 13 (LCMV cl13).

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

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

7 oire is broad and remains stable after acute LCMV infection, but it contracts and is narrower during

8 memory CD8 T cells generated after an acute LCMV infection.

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

10 pecific CD8(+) T cells dominate during acute LCMV infection and are predominantly exhausted during ch

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

12 In contrast, during acute LCMV infection, the TCR repertoire was much broader in b

13 imal antiviral T cell responses during acute LCMV infection.

14 However, following acute LCMV infection, in which PD-1 expression levels return t

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

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

17 However, Treg cell numbers collapsed after LCMV inoculation.

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

19 able as APCs for protective immunity against LCMV infection.

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

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

22 lear infection by coronavirus, influenza and LCMV in vivo.

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

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

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

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

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

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

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

41 Active chronic LCMV infection had a profound effect on total numbers, p

42 at function as resource cells during chronic LCMV infection and provide the proliferative burst seen

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

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

45 During chronic LCMV infections, the repertoires started as diverse but

46 y exhausted subsets generated during chronic LCMV infections.

47 CD8 T cell subset during established chronic LCMV infection.IMPORTANCE CD8 TCR repertoires responding

48 ltimately compromised the control of chronic LCMV clone 13 infection.

49 We studied the impact of chronic LCMV infection on the phenotype and function of memory b

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

51 etwork analysis, we demonstrate that chronic LCMV infection of the GIT leads to dysregulated microbia

52 he Pdcd1 gene during acute, but not chronic, LCMV infection.

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

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

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

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

57 es of IFNbeta versus IFNalpha in controlling LCMV infection.

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

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

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

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

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

63 Exploiting LCMV as a model system, we demonstrate that TRIM21 uses

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 Vaccine-induced LCMV-specific T-cell responses in mice lacking IL-10 wer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 put screen to rapidly identify inhibitors of LCMV multiplication.

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

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

108 ata, Lercher et al. show in a mouse model of LCMV infection that type I interferon alters the express

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

110 1 p.i. increased the frequency and number of LCMV-specific CD8 T cells, resulting in increased in viv

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

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

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

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

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

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

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

118 3 (Cl-13) variant of the Armstrong strain of LCMV (rCl-13/LASV-GPC) exhibited Cl-13-like growth prope

119 after challenge with a persistent strain of LCMV.

120 infection with the Armstrong (Arm) strain of LCMV.

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

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

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

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

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

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

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

128 Anti-PD-L1 treatment during persistent LCMV infection restored NP396-specific T cell responses

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

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

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

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

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

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

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

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

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

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

139 ent in mice infected with Friend retrovirus, LCMV Clone 13, and in patients with chronic HCV infectio

140 RIP-LCMV islets express CXCL10 after isolation and maintain

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

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

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

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

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

146 bly, despite discontinuation of ruxolitinib, LCMV-infected Prf1 (-/-) mice exhibited enhanced surviva

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

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

149 epitope sequence and a normally subdominant LCMV epitope.

150 mory is generated in the context of systemic LCMV or VV infection, but we cannot rule out the possibi

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

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

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

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

155 further screen hundreds of crRNAs along the LCMV genome to evaluate how conservation and target RNA

156 We thus characterized the LCMV-specific CD8 TCR repertoires of stem-like and termi

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

158 While supporting viral control in the LCMV model, oligoclonality and more private of TCR reper

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

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

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

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

163 54 bound at 2.5 logs higher affinity to the LCMV receptor alpha-dystroglycan (alpha-DG) than v2.2 an

164 that recovered from acute infection with the LCMV Armstrong (Arm) strain survive.

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

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

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

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

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

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

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

172 lator of CD8(+) T cell-mediated responses to LCMV Clone 13 viral infection.

173 not further erode memory T cells specific to LCMV.

174 of 42 vaccine recipients mounted a transient LCMV vector-neutralizing Ab response.

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

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

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

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

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

180 a subsequent lethal challenge with wild-type LCMV.

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

182 tion and better control of viral burden upon LCMV infection but show exacerbated HSC activation under

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

184 their steady-state endocytic functions upon LCMV infection.

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

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

187 atically different in response to LPS versus LCMV infection.

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

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

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

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

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

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

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

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

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

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

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

199 ted with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13) are highly susceptible to mousepox

200 ice with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13), result in immune dysfunction that

201 ted with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13).

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

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

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

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

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

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

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

209 xhausted lymphocytic choriomeningitis virus (LCMV) epitope.

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

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

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

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

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

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

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

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

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

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

220 chronic lymphocytic choriomeningitis virus (LCMV) infection have defined a PD-1(+) Tcf-1(+) CD8(+) T

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

222 s during lymphocytic choriomeningitis virus (LCMV) infection in an IL-21-dependent manner.

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

224 chronic lymphocytic choriomeningitis virus (LCMV) infection to examine the TCR diversity and lineage

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

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

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

228 rsistent lymphocytic choriomeningitis virus (LCMV) infection, it was shown that checkpoint inhibitor

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

230 ses upon lymphocytic choriomeningitis virus (LCMV) infection, which affects the outcomes of these ani

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

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

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

240 train of lymphocytic choriomeningitis virus (LCMV) is extensively used as a model of chronic infectio

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

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

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

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

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

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

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

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

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

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

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

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

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

254 licating lymphocytic choriomeningitis virus (LCMV) vectors expressing the human cytomegalovirus antig

255 on acute Lymphocytic Choriomeningitis Virus (LCMV) WE and Vaccinia Virus (VV) infections with naive T

256 Lymphocytic choriomeningitis virus (LCMV) WE variant 2.2 (v2.2) generated a high level of th

257 against lymphocytic choriomeningitis virus (LCMV) were assessed in mice that express or lack IL-10.

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

259 IV, HPV, lymphocytic choriomeningitis virus (LCMV), and schistosomiasis to evade host immunity.

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

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

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

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

264 chronic lymphocytic choriomeningitis virus (LCMV), performed RNA sequencing and proteomics of liver

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

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

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

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

269 gered by lymphocytic choriomeningitis virus (LCMV).

270 ted with lymphocytic choriomeningitis virus (LCMV).

271 ion with lymphocytic choriomeningitis virus (LCMV).

272 VSV) and lymphocytic choriomeningitis virus (LCMV).

273 chronic lymphocytic choriomeningitis virus (LCMV).

274 enavirus lymphocytic choriomeningitis virus (LCMV).

275 ion with lymphocytic choriomeningitis virus (LCMV).

276 ion with lymphocytic choriomeningitis virus (LCMV).

277 e-strand lymphocytic choriomeningitis virus (LCMV).

278 train of lymphocytic choriomeningitis virus (LCMV).

279 such as lymphocytic choriomeningitis virus (LCMV).

280 ted with lymphocytic choriomeningitis virus (LCMV).

281 ice with lymphocytic choriomeningitis virus (LCMV).

282 ion with lymphocytic choriomeningitis virus (LCMV).

283 viruses: lymphocytic choriomeningitis virus (LCMV); influenza A virus (IAV); and vesicular stomatitis

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

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

286 ice with lymphocytic choriomeningitis virus (LCMV; strain Armstrong).

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 Mice infected with LCMV WE v54, which differed from v2.2 by a single amino

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

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

297 Here, we show that viral infection with LCMV results in type I IFN-dependent Treg cell loss that

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

299 nflammation 24 h after inoculating mice with LCMV.

300 mpared to those in mice infected solely with LCMV.