ライフサイエンスコーパス: MCMV

1 MCMV activates the IRE1-XBP1 pathway early post infectio

2 MCMV commandeers patrolling monocytes to mediate systemi

3 MCMV infection increased the expression of chemokines th

4 MCMV infection initially reduced the numbers of LCMV-spe

5 MCMV infection of tumors in STING-deficient mice resulte

6 MCMV mutants lacking M45 or expressing C-terminally trun

7 MCMV reactivation was observed in intratumoral perivascu

8 MCMV-induced natural killer cytotoxicity was dependent o

9 MCMV-memory NK cells did not display enhanced activation

10 A MCMV mutant lacking the PVR inhibitor was attenuated in

11 We found that acute MCMV infection increased rapid T cell recruitment to the

12 After MCMV infection, Ly49D augmented IFN-gamma production by

13 oduce high levels of IFN-gamma rapidly after MCMV infection.

14 mechanisms mediate T cell recruitment after MCMV infection.

15 both lymphoid and nonlymphoid tissues after MCMV infection.

16 and are beneficial for host defense against MCMV infection.

17 ed for NK cell-mediated host defense against MCMV infection.

18 itopes to vaccinate mice and protect against MCMV.

19 K cells showed diminished protection against MCMV infection and exhibited more apoptosis compared wit

20 ubset also confers better protection against MCMV infection compared with the NKR-P1B(+)Ly49H(+) subs

21 ignaling was required for protection against MCMV.

22 us, EBI3 dampens the immune response against MCMV infection, resulting in prolonged viral persistence

23 der to improve resistance strategies against MCMV, we focused on how the MCMV genome is translated, t

24 ly M45 gene provided no protection, although MCMV vectors expressing the high-avidity epitope SSIEFAR

25 t as effectively as WT memory NK cells in an MCMV challenge model.

26 liver ILC1s acquire adaptive features in an MCMV-specific manner.

27 The identification of an MCMV gene involved in cell rounding provides the basis f

28 on complete loss of genome replication of an MCMV mutant carrying a deletion of the ie3-specific exon

29 This prompted the construction of an MCMV mutant lacking ie611 but retaining the coding capac

30 transcripts prompted the construction of an MCMV mutant lacking ie611 but retaining the coding capac

31 We show here that replication of an MCMV mutant lacking m166 is also severely attenuated dur

32 Here we provide evidence that an MCMV m145 family member, m153, functions to stabilize ce

33 DCs infected with an MCMV strain encoding the gB498 epitope from HSV-1 were u

34 We found that human CMV- and MCMV-specific T cells displayed shared genetic programs,

35 of MCMV infection, the infectious dose, and MCMV gene expression but was independent of IFNAR1, IL-1

36 dispensable for protection against ECTV and MCMV, two well-established models of viral infection in

37 ablish CD8(+) T cell memory to influenza and MCMV infection.

38 nfection allows presentation of SIINFEKL and MCMV-derived Ags by different cells within the same anim

39 early cytokine responses to viruses such as MCMV, possibly through maintenance of Treg survival and

40 more complex with a persistent virus such as MCMV.

41 ivity to the technique, interactions between MCMV, a glycoprotein-specific primary antibody to MCMV,

42 NK cells, which can be directly activated by MCMV protein m157, preferentially proliferated during MC

43 ese viral receptors, the M33 GPCR carried by MCMV is an activator of CREB, NF-kappaB, and phospholipa

44 data indicate that activation of NK cells by MCMV provides early nonspecific protection against M. tu

45 n induction of STAT3 Y705 phosphorylation by MCMV.

46 ion, Ly49D augmented IFN-gamma production by MCMV-specific Ly49H(+) NK cells and preferentially promo

47 strate that MHC-I mimicry strategies used by MCMV to avoid NK cell control are biologically relevant

48 CASP8-deficient mice was reduced by chronic MCMV infection.

49 Here, we demonstrate that mouse CMV (MCMV) also down-regulates the surface PVR.

50 CD4 T cell responses specific for mouse CMV (MCMV) epitopes and use a major histocompatibility comple

51 The CC chemokine MCK-2 encoded by mouse CMV (MCMV) has an atypical structure consisting of a classic

52 a robust primary response during mouse CMV (MCMV) infection but do not require this signal for memor

53 However, mouse CMV (MCMV) infection recently was shown to bypass the require

54 The outcome of mouse CMV (MCMV) infection varies among different inbred mouse stra

55 During mouse CMV (MCMV) infection, we observed Rsad2 (which encodes Viperi

56 An example of this is the mouse CMV (MCMV) m166 protein, which restricts expression of the TN

57 Here, we report that the single mouse CMV (MCMV) protein, m154, downregulates multiple surface mole

58 Similarly, mouse CMV (MCMV) replication in vimentin knockout mice is significa

59 To counter this, mouse CMV (MCMV) rescues some MHC I molecules to engage inhibitory

60 pitope KCSRNRQYL, and show that a mouse CMV (MCMV) vector provides complete immune control of recombi

61 We have previously characterized mouse CMV (MCMV)-encoded immune-evasive IFN signaling inhibition an

62 We assessed the ability of mouse CMV (MCMV)-induced memory Ly49H(+) NK cells to respond to cha

63 ulators of innate defense against mouse CMV (MCMV).

64 numbers following infection with mouse CMV (MCMV).

65 its the early innate response to murine CMV (MCMV) but is essential for the optimal generation of vir

66 lanoma, we previously found that murine CMV (MCMV) delayed tumor growth and activated tumor-specific

67 ed an m1-m16-deleted recombinant murine CMV (MCMV) expressing Mycobacterium tuberculosis Ag 85A to sh

68 in recipient mice infected with murine CMV (MCMV) expressing the cognate Ag OVA.

69 erized the role of the conserved murine CMV (MCMV) gene M79.

70 in some experimental situations, murine CMV (MCMV) infection delays tumor growth.

71 immune defense against human and murine CMV (MCMV) infection.

72 inct phases of activation during murine CMV (MCMV) infection: a nonselective phase mediated by proinf

73 atumoral injections of wild-type murine CMV (MCMV) into B16-F0 melanomas caused tumor growth delay in

74 served, as a similar sequence in murine CMV (MCMV) intron A was found to interact with CTCF and simil

75 Here, we used the murine CMV (MCMV) model of infection to determine that IFITM3 limits

76 V infections is reflected in the murine CMV (MCMV) model.

77 s to characterize the effects of murine CMV (MCMV) on GBM growth in murine models.

78 human cytomegalovirus (HCMV) and murine CMV (MCMV) prevents the activation of caspase-8 and proapopto

79 essing NK cells are essential to murine CMV (MCMV) resistance in MA/My mice.

80 imilar DNA sequence was found in murine CMV (MCMV) that is required for CTCF to bind to MCMV MIE gene

81 e that were infected or not with murine CMV (MCMV), a herpesvirus that infects the salivary gland and

82 Murine CMV (MCMV), which contains numerous gene segments highly simi

83 ell types that are infected with murine CMV (MCMV).

84 e this, we designed recombinant murine CMVs (MCMVs) encoding a SIINFEKL-enhanced GFP fusion protein u

85 LCMV-specific memory T cells, but continued MCMV persistence did not further erode memory T cells sp

86 d G2(+) NK cells might recognize and control MCMV infection.

87 rotected from lethal mousepox and controlled MCMV titers in the spleen.

88 f deletion mutants of mouse cytomegalovirus (MCMV) a mutant was identified that did not elicit cell r

89 ne cells critical for mouse cytomegalovirus (MCMV) clearance.

90 nd mice infected with mouse cytomegalovirus (MCMV) displayed elevated titers in the spleen.

91 The mouse cytomegalovirus (MCMV) immediate early 3 protein (611 amino acids; pIE611

92 Transcription of mouse cytomegalovirus (MCMV) immediate early ie1 and ie3 is controlled by the m

93 e NK cell response to mouse cytomegalovirus (MCMV) infection by comparing the activation and differen

94 vated NK cells during mouse cytomegalovirus (MCMV) infection in response to signals from the proinfla

95 Mouse cytomegalovirus (MCMV) infection promotes a rapid host-mediated loss of t

96 Early during mouse cytomegalovirus (MCMV) infection, NK cells up-regulated Adrb2 (which enco

97 mouse NK cells during mouse cytomegalovirus (MCMV) infection.

98 cell formation after mouse cytomegalovirus (MCMV) infection.

99 ting host response to mouse cytomegalovirus (MCMV) infection.

100 ed memory cells after mouse cytomegalovirus (MCMV) infection; therefore, we examined the role of Bim

101 AIM2 inflammasome by mouse cytomegalovirus (MCMV) or transfected double-stranded DNA did not require

102 epitopes derived from mouse cytomegalovirus (MCMV) that are recognized by CD4 T cells in BALB/c mice,

103 rine betaherpesvirus, mouse cytomegalovirus (MCMV).

104 ion of infection with mouse cytomegalovirus (MCMV).

105 persistent viruses, murine cytomegalovirus (MCMV) and lymphocytic choriomeningitis virus (LCMV; Cl13

106 host immune system, murine cytomegalovirus (MCMV) encodes three proteins that modulate cell surface

107 mic infection with a murine cytomegalovirus (MCMV) engineered to express HEL induced extensive prolif

108 xpressing individual murine cytomegalovirus (MCMV) genes protected mice against a lethal MCMV challen

109 f cytomegaloviruses, murine cytomegalovirus (MCMV) has been used as a model for in vivo studies of HC

110 ed susceptibility to murine cytomegalovirus (MCMV) infection.

111 microglia following murine cytomegalovirus (MCMV) infection.

112 ollision of a single murine cytomegalovirus (MCMV) on a platinum ultramicroelectrode (UME, radius of

113 hastic collisions of murine cytomegalovirus (MCMV) on ultramicroelectrodes (UMEs), extending the obse

114 tural mouse pathogen murine cytomegalovirus (MCMV) or the human pathogen herpes simplex virus-1 compa

115 espond to a specific murine cytomegalovirus (MCMV) protein and that in the absence of T and B cells,

116 tudy, we report that murine cytomegalovirus (MCMV) protein pM92 regulates viral late gene expression

117 Murine cytomegalovirus (MCMV) rapidly induces activation of nuclear factor kappa

118 g primary infection, murine cytomegalovirus (MCMV) spreads systemically, resulting in virus replicati

119 In this study, murine cytomegalovirus (MCMV) was used as a persistent infection model to study

120 Here we show that murine cytomegalovirus (MCMV), a prototypic beta-herpesvirus, harnesses the UPR

121 edly enhanced by the murine cytomegalovirus (MCMV)-encoded CC chemokine, MCK2, which promotes recruit

122 Interrogation of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necro

123 This murine cytomegalovirus (MCMV)-encoded protein, m12, restrains NK cell effector f

124 tis virus (LCMV) and murine cytomegalovirus (MCMV).

125 the beta-herpesvirus murine cytomegalovirus (MCMV).

126 K cells in a mouse model of cytomegalovirus (MCMV) infection.

127 spread was not needed and a spread-defective MCMV strain was equally effective.

128 Moreover, infections using m153-deficient MCMV mutants (Deltam144-m158 and Deltam153) show an acce

129 Using Deltaie611 MCMV, we demonstrated the dispensability of the canonica

130 Using Deltaie611 MCMV, we demonstrated the dispensability of the canonica

131 of infection with m157-deletant (Deltam157) MCMV was improved in mice carrying H-2 molecules unrecog

132 During MCMV infection, NK cells required MyD88, but not IL-1R,

133 During MCMV infection, the NKR-P1B(-)Ly49H(+) NK cell subset pr

134 induction and chromatin accessibility during MCMV infection.

135 tions to stabilize cell surface Clr-b during MCMV infection.

136 In contrast, during MCMV infection, NK cell responses to cytokines remained

137 e of pIE611 for viral gene expression during MCMV infection in an unbiased global approach, we used l

138 MV-specific TM retain memory function during MCMV infection and can re-establish CMV immunity when ne

139 ell recruitment to the salivary gland during MCMV infection.

140 impaired NK cell expansion and memory during MCMV challenge, in part due to a diminished proliferativ

141 icient (Ebi3(-/-) ) C57BL/6 (B6) mice during MCMV infection.

142 ein m157, preferentially proliferated during MCMV infection but did not show enhanced IFN-gamma produ

143 wild-type mice, and depletion of Treg during MCMV infection in Foxp3-diphtheria toxin receptor mice o

144 owed preferential proliferation during early MCMV infection.

145 RQYL is expressed within the immediate-early MCMV gene ie2 The same epitope expressed within the earl

146 viral loads following a challenge in elderly MCMV-infected animals and also reduced the differentiati

147 tion and a subunit vaccine approach elicited MCMV-specific and protective immunity.

148 n intensifies MCMV immunopathology, enhances MCMV burden in multiple organs, and suppresses MCMV-spec

149 erfusion with tcMCMV or adenovirus expressed MCMV proteins induced a 2- to 6-fold increase in systemi

150 When MCMV infection was given first (MCMV+LCMV), the magnitude of the acute T cell response t

151 Mice were evaluated for MCMV-specific antibodies, T-cell responses, germinal cen

152 ive immune responses were also necessary for MCMV to delay tumor growth as the effect was substantial

153 protein allowed differentiation of MCMV from MCMV bound by antibody from the collision frequency decr

154 ccelerated virus clearance and recovery from MCMV infection.

155 Fs m131 and m129 MCK-2 is essential for full MCMV infectivity in macrophages and for persistent infec

156 Furthermore, MCMV infection altered the functional state of macrophag

157 tudy solves a long-standing conundrum of how MCMV avoids recognition by NK cells, unravels a fundamen

158 estigating the role of the cytokine IL-22 in MCMV infection, we discovered an unanticipated function

159 Rapid NF-kappaB activation was absent in MCMV-infected NEMO-deficient fibroblasts, indicating tha

160 umor vasculature was strikingly augmented in MCMV+ mice.

161 NK cell depletion in MCMV-infected transplants also improves histology.

162 d that tumor growth was markedly enhanced in MCMV+ mice, with a significant reduction in overall surv

163 M2 phenotype in the absence of FcgammaRs in MCMV-infected Fcer1g and FcgR2b knockout mice.

164 creased angiogenesis and tumor blood flow in MCMV+ mice.

165 ication in spleen and liver were observed in MCMV-infected Ebi3(-/-) and wild-type (WT) B6 mice.

166 A similar phenotype in MCMV-infected Clr-b-deficient mice, which lack the ligan

167 ntiviral drug cidofovir improved survival in MCMV+ mice, inhibiting MCMV reactivation, PDGF-D express

168 n-deficient adenovirus expressing individual MCMV genes (gB, gH, IE1; controls: saline and replicatio

169 improved survival in MCMV+ mice, inhibiting MCMV reactivation, PDGF-D expression, pericyte recruitme

170 at the history of LCMV infection intensifies MCMV immunopathology, enhances MCMV burden in multiple o

171 n on the vascular endothelium and interrupts MCMV dissemination to the salivary glands independent of

172 Using a one-of-a-kind MCMV mutant unable to restrict expression of the TNF-rel

173 ne to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology, enhanced vi

174 r formation, and protection against a lethal MCMV challenge.

175 (MCMV) genes protected mice against a lethal MCMV challenge.

176 ector NK cells to generate a pool of mature, MCMV-specific memory cells.

177 Bone marrow chimeras revealed STING-mediated MCMV control in hematological cells, similar to MyD88.

178 Moreover, MCMV infection of macrophages drove them toward a proinf

179 - to 6-fold increase in systemic and mucosal MCMV-specific antibodies, a 3- to 6-fold increase in GC

180 th naive cells when challenged with a mutant MCMV lacking m157, highlighting their antigen-specific r

181 These results highlight a novel MCMV-mediated immune evasion strategy.

182 ashion in the steady-state in the absence of MCMV or any infection.

183 K cells and subsequently impaired control of MCMV replication.

184 ized and antigen-specific for the control of MCMV upon rechallenge.

185 sponse was sufficient for initial control of MCMV, although at later time points, CD70(-/-) mice beca

186 lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral repl

187 However, costimulation of MCMV-memory NK cells with IL-12 and m157 antigen rescues

188 urther apply this method to the detection of MCMV in urine of infected mice.

189 -1 (Nrp-1) emerge as crucial determinants of MCMV infection.

190 face glycoprotein allowed differentiation of MCMV from MCMV bound by antibody from the collision freq

191 -MHC class I modulate the differentiation of MCMV-specific NK cells and are beneficial for host defen

192 phosphorylation depended on the duration of MCMV infection, the infectious dose, and MCMV gene expre

193 In most mice, the antitumor effect of MCMV was transient.

194 active and document antagonistic effects of MCMV on STAT1/3-dependent target gene expression.

195 Although the effects of MCMV on tumor growth were transient, we found that repea

196 e responses to H-2(d)-restricted epitopes of MCMV pp89 and M18 Ags characteristic of infection with o

197 at EBI3 plays a role in the establishment of MCMV latency.

198 ockade of DNAM-1 suppressed the expansion of MCMV-specific Ly49H(+) cells during viral infection and

199 1 played distinct roles in the generation of MCMV-specific effector and memory NK cells.

200 ized the translation initiation mechanism of MCMV.

201 many of these could promote the migration of MCMV-specific T cells in vitro.

202 s and highlight the complex orchestration of MCMV gene regulation.

203 cytokine response during the early phase of MCMV infection in CD70(-/-) mice was paralleled by a red

204 is a key determinant of the initial phase of MCMV infection.

205 The m20.1 protein of MCMV retains PVR in the endoplasmic reticulum and promot

206 as well as posttranscriptional regulation of MCMV gene products by pIE611.

207 and similarly function in the repression of MCMV MIE gene expression mediated by CTCF.

208 ypic changes a month after the resolution of MCMV infection, and showed an enhanced protective effect

209 However, an additional round of MCMV infection further delayed tumor growth, suggesting

210 nique domain, resulting from the splicing of MCMV ORFs m131 and m129 MCK-2 is essential for full MCMV

211 urden in multiple organs, and suppression of MCMV-specific T cell memory inflation.

212 CD4 T cells that recognize them to fight off MCMV infection, and show that we can use the epitopes to

213 s age-dependent decline was not dependent on MCMV.

214 ary glands via Wharton's duct with tcMCMV or MCMV proteins focused to the salivary gland via replicat

215 8 Ags characteristic of infection with other MCMVs.

216 uggesting that this DC subset cross-presents MCMV-encoded Ag in vivo.

217 gocytes with clodronate completely prevented MCMV from delaying tumor growth.

218 ve response between a newly defined putative MCMV epitope sequence and a normally subdominant LCMV ep

219 ss-reactive between a newly defined putative MCMV epitope sequence, M57727-734, and the normally subd

220 vaccination of immunocompetent mice reduced MCMV replication in the same organs where CD4 cytotoxic

221 rowth were transient, we found that repeated MCMV injections sustained the antitumor effect, suggesti

222 for CTCF to bind to MCMV MIE gene to repress MCMV MIE gene expression.

223 though STAT3 phosphorylation did not require MCMV immediate early 1, pM27, and late gene expression,

224 lymphocyte response by 80%, and the residual MCMV tetramer-specific lymphocytes exhibited a less diff

225 MV burden in multiple organs, and suppresses MCMV-specific T cell memory inflation.

226 Surprisingly, MCMV-specific memory inflation was not sustained long-te

227 sequence, we show that some of the long-term MCMV-immune mice mount a robust CD8 T cell cross-reactiv

228 We demonstrate that MCMV-specific CD4 T cells can express high levels of gra

229 r analysis to STAT1 and STAT3, we found that MCMV infection neither destabilizes STAT1 protein nor pr

230 by IL-6 was also abolished, indicating that MCMV antagonizes STAT1 and STAT3 despite the occurrence

231 We report that MCMV RNA contains a cap-independent translation element

232 These findings reveal that MCMV-primed memory NK cells are diminished in their resp

233 We now show that MCMV acts as a STING agonist in the tumor.

234 Here, we show that MCMV delayed the growth of these immunologically "cold"

235 We now show that MCMV delayed tumor growth through a mechanism that requi

236 Together, our studies show that MCMV epitope-specific CD4 T cells have the potential to

237 Overall, these data show that MCMV infection and sensing in tumor-associated macrophag

238 These data show that MCMV potentiates GBM growth in vivo by increased pericyt

239 Previously, we have shown that MCMV protein pM79 and its human cytomegalovirus (HCMV) h

240 Together, our results suggest that MCMV infection delayed the growth of an immunologically

241 Mechanistically, our data suggest that MCMV recruits new macrophages to the tumor via the virus

242 The MCMV 3' CITE (MTE) was mapped to nucleotides 4164 to 433

243 The MCMV genome, like the genomes of other beta- and gammahe

244 The MCMV-specific TM population was stable over time and ret

245 After a transient phase of activation, the MCMV M45 protein blocks all canonical NF-kappaB-activati

246 Although the MCMV genome encodes for MHC class I-homologous decoy lig

247 the appearance of NK cells that express the MCMV-specific receptor Ly49H.

248 rategies against MCMV, we focused on how the MCMV genome is translated, the first step of gene expres

249 nd oral lavage was strongly decreased in the MCMV-infected Ebi3(-/-) B6 mice, suggesting that EBI3 pl

250 cells and lower serum levels of IL-10 in the MCMV-infected Ebi3(-/-) B6 mice.

251 to delineate pIE611-dependent changes of the MCMV proteome.

252 d delineated pIE611-dependent changes of the MCMV proteome.

253 Treatment reduced the magnitude of the MCMV-specific CD8(+) T-lymphocyte response by 80%, and t

254 Memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, and were independent of b

255 e examined the role of Bim in regulating the MCMV-driven memory NK cell pool.

256 ayed shared genetic programs, validating the MCMV model for studies of CMV-specific T cells in vivo.

257 However, some of these MCMV persistently infected mice with acute LCMV infectio

258 Thus, MCMV altered tumor growth by actively recruiting macroph

259 a glycoprotein-specific primary antibody to MCMV, and polystyrene bead "anchors," which were functio

260 (MCMV) that is required for CTCF to bind to MCMV MIE gene to repress MCMV MIE gene expression.

261 rapidly responding population of NK cells to MCMV infection, but are highly regulated by Tregs and TG

262 Thus, MyD88 and STING contribute to MCMV control in distinct cell types that initiate downst

263 n and memory formation following exposure to MCMV, in part because of greater apoptosis.

264 own resistance genes that confer immunity to MCMV.

265 n, and both can contribute nonredundantly to MCMV defense, revealing that these two innate lymphocyte

266 CD70(-/-) mice reacted to MCMV infection with a robust type I IFN and proinflammat

267 killer (NK) cells and stronger resistance to MCMV.

268 engineering of-or breeding for-resistance to MCMV.

269 ess tissue damage, and greater resistance to MCMV.

270 The higher peak response to MCMV in Casp8 (-/-) Ripk3 (-/-) mice resulted from accum

271 By examining the NK cell response to MCMV infection in novel BALB substrains congenic for dif

272 composition of the inflationary response to MCMV.

273 cytometry to visualize the host response to MCMV.

274 ism, transcription or antiviral responses to MCMV infection.

275 d late gene expression, it was restricted to MCMV-infected cells and not transmitted to bystander cel

276 s, CD70(-/-) mice became more susceptible to MCMV infection.

277 a beta2-AR agonist were more susceptible to MCMV infection.

278 e as immune-privileged vehicles to transport MCMV via the bloodstream to distal organs.

279 We previously showed that wild-type MCMV delayed the growth of poorly immunogenic B16 melano

280 actin cytoskeleton observed after wild-type MCMV infection, and isolated expression of the M25 prote

281 In this model, wild-type MCMV, lacking HEL, did not induce overt uveitis, suggest

282 found decreasing STAT3 protein amounts upon MCMV infection, although STAT3 expression normally is po

283 dendritic cells activated only NK cells upon MCMV infection, consistent with their virtual lack of IL

284 the early control of and host survival upon MCMV infection but not the long-term control of LCMV inf

285 Maize chlorotic mottle virus (MCMV) combines with a potyvirus in maize lethal necrosis

286 Maize chlorotic mottle virus (MCMV) infection is required for this disease.

287 Ex vivo, MCMV-memory NK cells displayed reduced phosphorylation o

288 When MCMV infection was given first (MCMV+LCMV), the magnitud

289 t data highlight a unique mechanism by which MCMV modulates NK ligand expression.IMPORTANCE Cytomegal

290 ffector response to secondary challenge with MCMV consistent with a memory lymphocyte response.

291 his response was more highly correlated with MCMV control than all other immune cell features.

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

293 implanted in mice perinatally infected with MCMV versus controls.

294 tion in the natural mouse host infected with MCMV, in settings where virus-specific CD8 T cells are a

295 s abolished in IL-12(-/-) mice infected with MCMV, whereas NK cells were still activated.

296 stablished in mice perinatally infected with MCMV.

297 isplay at individual sites of infection with MCMV.

298 n proliferation during latent infection with MCMV.

299 and replication deficient adenovirus without MCMV inserts).

300 e and extent of aggregation with and without MCMV.