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1                                              MCMV activated the PERK-ATF4 pathway but only induced a
2                                              MCMV commandeers patrolling monocytes to mediate systemi
3                                              MCMV D+/R- and D-/R- allogeneic transplants were perform
4                                              MCMV infection exacerbates late renal allograft damage a
5                                              MCMV infection increased phosphorylated STAT3 (p-STAT3)
6                                              MCMV infection increased the expression of chemokines th
7                                              MCMV infection initially reduced the numbers of LCMV-spe
8                                              MCMV mutants lacking M45 or expressing C-terminally trun
9                                              MCMV-infected grafts contained greater frequencies of NK
10                                              MCMV-infected Mut3 mice exhibited a shorter survival tim
11                                              MCMV-memory NK cells did not display enhanced activation
12                                   At day 42, MCMV-infected transplants had higher damage scores (15.6
13                                            A MCMV mutant lacking the PVR inhibitor was attenuated in
14 increased IFN-gamma was evident during acute MCMV infection in vivo.
15                          We found that acute MCMV infection increased rapid T cell recruitment to the
16 operly through TLR3, TLR7 and TLR9, to acute MCMV infection to determine whether liver antiviral defe
17                                        After MCMV infection, Ly49D augmented IFN-gamma production by
18 oid and nonlymphoid tissues for months after MCMV infection, IL-12 receptor-deficient NK cells failed
19  and were unable to mediate protection after MCMV challenge.
20 oduce high levels of IFN-gamma rapidly after MCMV infection.
21  mechanisms mediate T cell recruitment after MCMV infection.
22  both lymphoid and nonlymphoid tissues after MCMV infection.
23 ed for NK cell-mediated host defense against MCMV infection.
24  and are beneficial for host defense against MCMV infection.
25 K cells in C57L mice fail to protect against MCMV infection.
26 itopes to vaccinate mice and protect against MCMV.
27 K cells showed diminished protection against MCMV infection and exhibited more apoptosis compared wit
28 ubset also confers better protection against MCMV infection compared with the NKR-P1B(+)Ly49H(+) subs
29 us, EBI3 dampens the immune response against MCMV infection, resulting in prolonged viral persistence
30 ly M45 gene provided no protection, although MCMV vectors expressing the high-avidity epitope SSIEFAR
31 t as effectively as WT memory NK cells in an MCMV challenge model.
32                     The identification of an MCMV gene involved in cell rounding provides the basis f
33 on complete loss of genome replication of an MCMV mutant carrying a deletion of the ie3-specific exon
34         This prompted the construction of an MCMV mutant lacking ie611 but retaining the coding capac
35  transcripts prompted the construction of an MCMV mutant lacking ie611 but retaining the coding capac
36                         DCs infected with an MCMV strain encoding the gB498 epitope from HSV-1 were u
37                 We found that human CMV- and MCMV-specific T cells displayed shared genetic programs,
38  of MCMV infection, the infectious dose, and MCMV gene expression but was independent of IFNAR1, IL-1
39 ablish CD8(+) T cell memory to influenza and MCMV infection.
40 nfection allows presentation of SIINFEKL and MCMV-derived Ags by different cells within the same anim
41 MV UL128 homologue) and r131 (HCMV UL130 and MCMV m129/130 homologues).
42 subsets on anti-murine cytomegalovirus (anti-MCMV) responses after syngeneic hematopoietic stem cell
43  early cytokine responses to viruses such as MCMV, possibly through maintenance of Treg survival and
44 more complex with a persistent virus such as MCMV.
45 ivity to the technique, interactions between MCMV, a glycoprotein-specific primary antibody to MCMV,
46 NK cells, which can be directly activated by MCMV protein m157, preferentially proliferated during MC
47 ese viral receptors, the M33 GPCR carried by MCMV is an activator of CREB, NF-kappaB, and phospholipa
48 data indicate that activation of NK cells by MCMV provides early nonspecific protection against M. tu
49 n induction of STAT3 Y705 phosphorylation by MCMV.
50   Here, we identify a transcript produced by MCMV that binds to miR-27 and mediates its degradation.
51 ion, Ly49D augmented IFN-gamma production by MCMV-specific Ly49H(+) NK cells and preferentially promo
52 strate that MHC-I mimicry strategies used by MCMV to avoid NK cell control are biologically relevant
53         Here, we demonstrate that mouse CMV (MCMV) also down-regulates the surface PVR.
54 CD4 T cell responses specific for mouse CMV (MCMV) epitopes and use a major histocompatibility comple
55 ia monocytogenes by a recombinant mouse CMV (MCMV) expressing the NKG2D ligand retinoic acid early-in
56 The CC chemokine MCK-2 encoded by mouse CMV (MCMV) has an atypical structure consisting of a classic
57  a robust primary response during mouse CMV (MCMV) infection but do not require this signal for memor
58                          However, mouse CMV (MCMV) infection recently was shown to bypass the require
59 of direct versus cross priming in mouse CMV (MCMV) infection using recombinant viruses.
60                    The outcome of mouse CMV (MCMV) infection varies among different inbred mouse stra
61 ed for immune-mediated control of mouse CMV (MCMV) infection.
62 pitope KCSRNRQYL, and show that a mouse CMV (MCMV) vector provides complete immune control of recombi
63  We have previously characterized mouse CMV (MCMV)-encoded immune-evasive IFN signaling inhibition an
64        We assessed the ability of mouse CMV (MCMV)-induced memory Ly49H(+) NK cells to respond to cha
65 ulators of innate defense against mouse CMV (MCMV).
66 its the early innate response to murine CMV (MCMV) but is essential for the optimal generation of vir
67 ed an m1-m16-deleted recombinant murine CMV (MCMV) expressing Mycobacterium tuberculosis Ag 85A to sh
68 erized the role of the conserved murine CMV (MCMV) gene M79.
69 ry inflation, first described in murine CMV (MCMV) infection, is characterized by the accumulation of
70  months in mice with established murine CMV (MCMV) infection.
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 served, as a similar sequence in murine CMV (MCMV) intron A was found to interact with CTCF and simil
74                Here, we used the murine CMV (MCMV) model of infection to determine that IFITM3 limits
75 V infections is reflected in the murine CMV (MCMV) model.
76 toma, we assessed the effects of murine CMV (MCMV) perinatal infection in a GFAP-cre; Nf1(loxP/+); Tr
77                            Using murine CMV (MCMV) recombinants expressing a single CD8 T cell epitop
78                             In a murine CMV (MCMV) renal transplantation model, ganciclovir prophylax
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 demonstrate that infections with murine CMV (MCMV), but not with lymphocytic choriomeningitis virus,
83 ity against the mouse homologue, murine CMV (MCMV), in lethally irradiated mice given allogeneic puri
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  beyond their recognized role in controlling MCMV replication, NK cells preserve organ integrity and
88 by the mouse innate immune system to counter MCMV.
89 f deletion mutants of mouse cytomegalovirus (MCMV) a mutant was identified that did not elicit cell r
90 -stranded DNA viruses mouse cytomegalovirus (MCMV) and human adenovirus.
91 ne cells critical for mouse cytomegalovirus (MCMV) clearance.
92                   The mouse cytomegalovirus (MCMV) immediate early 3 protein (611 amino acids; pIE611
93      Transcription of mouse cytomegalovirus (MCMV) immediate early ie1 and ie3 is controlled by the m
94 e NK cell response to mouse cytomegalovirus (MCMV) infection by comparing the activation and differen
95 vated NK cells during mouse cytomegalovirus (MCMV) infection in response to signals from the proinfla
96                During mouse cytomegalovirus (MCMV) infection, the first wave of type I interferon (IF
97 mouse NK cells during mouse cytomegalovirus (MCMV) infection.
98  cell formation after mouse cytomegalovirus (MCMV) infection.
99 ed memory cells after mouse cytomegalovirus (MCMV) infection; therefore, we examined the role of Bim
100 -) mice infected with mouse cytomegalovirus (MCMV) or recombinant viruses expressing the viral m157 g
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 red for resistance to mouse cytomegalovirus (MCMV), as identified through unbiased genetic screening.
104    In infections with mouse cytomegalovirus (MCMV), MCMV-specific NK cells undergo clonal expansion,
105 e recent studies: (i) mouse cytomegalovirus (MCMV)-induced memory; (ii) cytokine-induced memory; and
106  is indispensible for mouse cytomegalovirus (MCMV)-specific NK cell expansion and generation of memor
107 rine betaherpesvirus, mouse cytomegalovirus (MCMV).
108 s were infected with murine cytomegalovirus (MCMV) after birth at 2 days (P2) or 4 weeks of age and t
109  persistent viruses, murine cytomegalovirus (MCMV) and lymphocytic choriomeningitis virus (LCMV; Cl13
110  host immune system, murine cytomegalovirus (MCMV) encodes three proteins that modulate cell surface
111 mic infection with a murine cytomegalovirus (MCMV) engineered to express HEL induced extensive prolif
112 f cytomegaloviruses, murine cytomegalovirus (MCMV) has been used as a model for in vivo studies of HC
113  of mouse cells with murine cytomegalovirus (MCMV) induces the rapid down-regulation of an antiviral
114  necrosis induced by murine cytomegalovirus (MCMV) infection or death receptor activation and suppres
115                      Murine cytomegalovirus (MCMV) infection severely impaired saliva secretion indep
116 ed susceptibility to murine cytomegalovirus (MCMV) infection.
117  microglia following murine cytomegalovirus (MCMV) infection.
118 tently infected with murine cytomegalovirus (MCMV) into NOD.Cg-Prkdc(scid) IL2rg(tm1Wjl) /Szj mice re
119 e hepatotropic virus murine cytomegalovirus (MCMV) involves complex cytokine and cellular interaction
120 ollision of a single murine cytomegalovirus (MCMV) on a platinum ultramicroelectrode (UME, radius of
121 hastic collisions of murine cytomegalovirus (MCMV) on ultramicroelectrodes (UMEs), extending the obse
122 espond to a specific murine cytomegalovirus (MCMV) protein and that in the absence of T and B cells,
123 tudy, we report that murine cytomegalovirus (MCMV) protein pM92 regulates viral late gene expression
124                      Murine cytomegalovirus (MCMV) rapidly induces activation of nuclear factor kappa
125 odel of experimental murine cytomegalovirus (MCMV) retinitis in mice with retrovirus-induced immunosu
126 g primary infection, murine cytomegalovirus (MCMV) spreads systemically, resulting in virus replicati
127       In this study, murine cytomegalovirus (MCMV) was used as a persistent infection model to study
128 he protease (mPR) of murine cytomegalovirus (MCMV), which is essential for viral replication.
129 edly enhanced by the murine cytomegalovirus (MCMV)-encoded CC chemokine, MCK2, which promotes recruit
130     Interrogation of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necro
131                 This murine cytomegalovirus (MCMV)-encoded protein, m12, restrains NK cell effector f
132 tis virus (LCMV) and murine cytomegalovirus (MCMV).
133 K cells in a mouse model of cytomegalovirus (MCMV) infection.
134                             Using Deltaie611 MCMV, we demonstrated the dispensability of the canonica
135                             Using Deltaie611 MCMV, we demonstrated the dispensability of the canonica
136  of infection with m157-deletant (Deltam157) MCMV was improved in mice carrying H-2 molecules unrecog
137 T cell epitope from HSV-1 fused to different MCMV genes, we show that magnitude and kinetics of T cel
138                                       During MCMV infection, NK cells required MyD88, but not IL-1R,
139                                       During MCMV infection, the NKR-P1B(-)Ly49H(+) NK cell subset pr
140 gamma compared with Sca-1(-) NK cells during MCMV infection.
141                          In contrast, during MCMV infection, NK cell responses to cytokines remained
142 omoting early liver antiviral defense during MCMV infection.
143  (as well as KLRG1) on NK cells early during MCMV infection, differential expression of Sca-1, as wel
144  in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also d
145      The numbers of NK cells elicited during MCMV infection are reduced by IL-2 neutralization.
146 e of pIE611 for viral gene expression during MCMV infection in an unbiased global approach, we used l
147 MV-specific TM retain memory function during MCMV infection and can re-establish CMV immunity when ne
148 ell recruitment to the salivary gland during MCMV infection.
149 n Ly49H(+) and Ly49H(-) NK cells late during MCMV infection.
150 icient (Ebi3(-/-) ) C57BL/6 (B6) mice during MCMV infection.
151 ein m157, preferentially proliferated during MCMV infection but did not show enhanced IFN-gamma produ
152 wild-type mice, and depletion of Treg during MCMV infection in Foxp3-diphtheria toxin receptor mice o
153 d T cells specific for nonrecombinant (i.e., MCMV-derived) Ags.
154 owed preferential proliferation during early MCMV infection.
155 RQYL is expressed within the immediate-early MCMV gene ie2 The same epitope expressed within the earl
156 viral loads following a challenge in elderly MCMV-infected animals and also reduced the differentiati
157 tion and a subunit vaccine approach elicited MCMV-specific and protective immunity.
158  the number of cells specific for endogenous MCMV Ags.
159  in a depressed early response to endogenous MCMV Ag.
160 depression of immune responses to endogenous MCMV Ags.
161 n intensifies MCMV immunopathology, enhances MCMV burden in multiple organs, and suppresses MCMV-spec
162 erfusion with tcMCMV or adenovirus expressed MCMV proteins induced a 2- to 6-fold increase in systemi
163         When MCMV infection was given first (MCMV+LCMV), the magnitude of the acute T cell response t
164                      Mice were evaluated for MCMV-specific antibodies, T-cell responses, germinal cen
165 protein allowed differentiation of MCMV from MCMV bound by antibody from the collision frequency decr
166 ccelerated virus clearance and recovery from MCMV infection.
167 Fs m131 and m129 MCK-2 is essential for full MCMV infectivity in macrophages and for persistent infec
168 ficient hosts provided significantly greater MCMV resistance compared with transfer of total NK popul
169 leomorphic rhabdomyosarcomas (RMS) harboring MCMV DNA, RNA, and protein.
170 estigating the role of the cytokine IL-22 in MCMV infection, we discovered an unanticipated function
171     Rapid NF-kappaB activation was absent in MCMV-infected NEMO-deficient fibroblasts, indicating tha
172                                        As in MCMV, only the inflating epitope showed immunoproteasome
173                         NK cell depletion in MCMV-infected transplants also improves histology.
174  contributed minimally to retinal disease in MCMV-infected eyes of MAIDS-10 mice.
175  M2 phenotype in the absence of FcgammaRs in MCMV-infected Fcer1g and FcgR2b knockout mice.
176 mPR expression and viral growth was found in MCMV-infected cells treated with Salmonella carrying the
177 vivo, there was increased p-STAT3 in NSCs in MCMV-infected compared with control mice.
178 ication in spleen and liver were observed in MCMV-infected Ebi3(-/-) and wild-type (WT) B6 mice.
179                       A similar phenotype in MCMV-infected Clr-b-deficient mice, which lack the ligan
180 type, and functions similar to those seen in MCMV and are reproduced using alternative routes of admi
181 n-deficient adenovirus expressing individual MCMV genes (gB, gH, IE1; controls: saline and replicatio
182                    Early on after infection, MCMV antigen was predominantly localized in CD45+ lympho
183 ch harbored equivalent amounts of infectious MCMV.
184 at the history of LCMV infection intensifies MCMV immunopathology, enhances MCMV burden in multiple o
185 n on the vascular endothelium and interrupts MCMV dissemination to the salivary glands independent of
186 ppression (MAIDS), we initially investigated MCMV-infected eyes for evidence of apoptosis-associated
187                          In addition, latent MCMV infection suppressed the proportion of naive CD8(+)
188 ne to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology, enhanced vi
189 r formation, and protection against a lethal MCMV challenge.
190 ector NK cells to generate a pool of mature, MCMV-specific memory cells.
191 nfections with mouse cytomegalovirus (MCMV), MCMV-specific NK cells undergo clonal expansion, and dis
192  evidence of apoptosis-associated molecules, MCMV-infected eyes of MAIDS-10 mice showed significant a
193                                    Moreover, MCMV induced ER chaperone Bip but actively blocked IRE1-
194 - to 6-fold increase in systemic and mucosal MCMV-specific antibodies, a 3- to 6-fold increase in GC
195 th naive cells when challenged with a mutant MCMV lacking m157, highlighting their antigen-specific r
196 rtantly, as with RIP3(-/-) mice, vIRA mutant MCMV pathogenesis is restored in DAI(-/-) mice, consiste
197 ashion in the steady-state in the absence of MCMV or any infection.
198 K cells and subsequently impaired control of MCMV replication.
199 ized and antigen-specific for the control of MCMV upon rechallenge.
200 sponse was sufficient for initial control of MCMV, although at later time points, CD70(-/-) mice beca
201  lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral repl
202                    However, costimulation of MCMV-memory NK cells with IL-12 and m157 antigen rescues
203 urther apply this method to the detection of MCMV in urine of infected mice.
204 face glycoprotein allowed differentiation of MCMV from MCMV bound by antibody from the collision freq
205 -MHC class I modulate the differentiation of MCMV-specific NK cells and are beneficial for host defen
206  phosphorylation depended on the duration of MCMV infection, the infectious dose, and MCMV gene expre
207  active and document antagonistic effects of MCMV on STAT1/3-dependent target gene expression.
208 e responses to H-2(d)-restricted epitopes of MCMV pp89 and M18 Ags characteristic of infection with o
209 at EBI3 plays a role in the establishment of MCMV latency.
210 ockade of DNAM-1 suppressed the expansion of MCMV-specific Ly49H(+) cells during viral infection and
211 on lymphopenia promoted massive expansion of MCMV-specific T cells when no competing donor T cells we
212 1 played distinct roles in the generation of MCMV-specific effector and memory NK cells.
213 ll depletion improved allograft histology of MCMV-infected grafts.
214  by 7 weeks, there was a generalized loss of MCMV in brain, confirmed by bioluminescent imaging.
215  will be useful in elucidating mechanisms of MCMV reactivation, including the roles of injury and of
216 many of these could promote the migration of MCMV-specific T cells in vitro.
217 s and highlight the complex orchestration of MCMV gene regulation.
218  cytokine response during the early phase of MCMV infection in CD70(-/-) mice was paralleled by a red
219 on on naive blood NK cells was predictive of MCMV resistance.
220                         The m20.1 protein of MCMV retains PVR in the endoplasmic reticulum and promot
221 as well as posttranscriptional regulation of MCMV gene products by pIE611.
222  and similarly function in the repression of MCMV MIE gene expression mediated by CTCF.
223 nique domain, resulting from the splicing of MCMV ORFs m131 and m129 MCK-2 is essential for full MCMV
224 urden in multiple organs, and suppression of MCMV-specific T cell memory inflation.
225 CD4 T cells that recognize them to fight off MCMV infection, and show that we can use the epitopes to
226 s age-dependent decline was not dependent on MCMV.
227 by 60% compared to antiviral-treated mice or MCMV-negative animals.
228 ary glands via Wharton's duct with tcMCMV or MCMV proteins focused to the salivary gland via replicat
229 8 Ags characteristic of infection with other MCMVs.
230               The majority of tumors from P2 MCMV-infected mice were pleomorphic rhabdomyosarcomas (R
231 uggesting that this DC subset cross-presents MCMV-encoded Ag in vivo.
232 ve response between a newly defined putative MCMV epitope sequence and a normally subdominant LCMV ep
233 ss-reactive between a newly defined putative MCMV epitope sequence, M57727-734, and the normally subd
234                 Infection with a recombinant MCMV inducing a vigorous initial immune response to the
235  vaccination of immunocompetent mice reduced MCMV replication in the same organs where CD4 cytotoxic
236 les of these two IFN-I sources in regulating MCMV defense remain unclear.
237 ticipate simultaneously during MAIDS-related MCMV retinitis, and all may play a role during AIDS-rela
238 for CTCF to bind to MCMV MIE gene to repress MCMV MIE gene expression.
239 though STAT3 phosphorylation did not require MCMV immediate early 1, pM27, and late gene expression,
240 lymphocyte response by 80%, and the residual MCMV tetramer-specific lymphocytes exhibited a less diff
241                                  Strikingly, MCMV production in the spleens of immunocompetent mice n
242 MV burden in multiple organs, and suppresses MCMV-specific T cell memory inflation.
243 sequence, we show that some of the long-term MCMV-immune mice mount a robust CD8 T cell cross-reactiv
244                          We demonstrate that MCMV-specific CD4 T cells can express high levels of gra
245          These observations demonstrate that MCMV-specific memory inflation is maintained by viral re
246         Subsequent studies demonstrated that MCMV-infected eyes of MAIDS-10 mice, but not MAIDS-4 mic
247 r analysis to STAT1 and STAT3, we found that MCMV infection neither destabilizes STAT1 protein nor pr
248  by IL-6 was also abolished, indicating that MCMV antagonizes STAT1 and STAT3 despite the occurrence
249                   These findings reveal that MCMV-primed memory NK cells are diminished in their resp
250              Together, our studies show that MCMV epitope-specific CD4 T cells have the potential to
251               Previously, we have shown that MCMV protein pM79 and its human cytomegalovirus (HCMV) h
252                                          The MCMV genome, like the genomes of other beta- and gammahe
253                                          The MCMV model is, however, complicated by the virus's low-l
254                                          The MCMV-specific TM population was stable over time and ret
255   After a transient phase of activation, the MCMV M45 protein blocks all canonical NF-kappaB-activati
256                                 Although the MCMV genome encodes for MHC class I-homologous decoy lig
257 th receptor activation and suppressed by the MCMV-encoded viral inhibitor of RIP activation (vIRA).
258  the appearance of NK cells that express the MCMV-specific receptor Ly49H.
259 nd oral lavage was strongly decreased in the MCMV-infected Ebi3(-/-) B6 mice, suggesting that EBI3 pl
260 cells and lower serum levels of IL-10 in the MCMV-infected Ebi3(-/-) B6 mice.
261 to delineate pIE611-dependent changes of the MCMV proteome.
262 d delineated pIE611-dependent changes of the MCMV proteome.
263       Treatment reduced the magnitude of the MCMV-specific CD8(+) T-lymphocyte response by 80%, and t
264 e examined the role of Bim in regulating the MCMV-driven memory NK cell pool.
265 ayed shared genetic programs, validating the MCMV model for studies of CMV-specific T cells in vivo.
266                       However, some of these MCMV persistently infected mice with acute LCMV infectio
267       Thus, while vulnerable at early times, MCMV became resistant to exogenous ER stress at late tim
268  a glycoprotein-specific primary antibody to MCMV, and polystyrene bead "anchors," which were functio
269               Thus, NK licensing behavior to MCMV corresponds to the donor, and not recipient, MHC ha
270  (MCMV) that is required for CTCF to bind to MCMV MIE gene to repress MCMV MIE gene expression.
271 rapidly responding population of NK cells to MCMV infection, but are highly regulated by Tregs and TG
272 ting the earliest phase of innate defense to MCMV infection, capping replication levels, and blocking
273 n, and both can contribute nonredundantly to MCMV defense, revealing that these two innate lymphocyte
274                    CD70(-/-) mice reacted to MCMV infection with a robust type I IFN and proinflammat
275         By examining the NK cell response to MCMV infection in novel BALB substrains congenic for dif
276  defects in expansion during the response to MCMV infection, suggesting that their regulation by miR-
277  composition of the inflationary response to MCMV.
278  cytometry to visualize the host response to MCMV.
279 ed to phosphorylate eIF2alpha in response to MCMV.
280 d late gene expression, it was restricted to MCMV-infected cells and not transmitted to bystander cel
281 howed a modest increase in susceptibility to MCMV infection, demonstrating that translational arrest
282 s, CD70(-/-) mice became more susceptible to MCMV infection.
283 e as immune-privileged vehicles to transport MCMV via the bloodstream to distal organs.
284  actin cytoskeleton observed after wild-type MCMV infection, and isolated expression of the M25 prote
285                     In this model, wild-type MCMV, lacking HEL, did not induce overt uveitis, suggest
286  found decreasing STAT3 protein amounts upon MCMV infection, although STAT3 expression normally is po
287 dendritic cells activated only NK cells upon MCMV infection, consistent with their virtual lack of IL
288  the early control of and host survival upon MCMV infection but not the long-term control of LCMV inf
289                                     Ex vivo, MCMV-memory NK cells displayed reduced phosphorylation o
290                                         When MCMV infection was given first (MCMV+LCMV), the magnitud
291                                         When MCMV-infected mice were orally treated with Salmonella c
292                                      Whereas MCMV-infected eyes of MAIDS-4 mice showed little evidenc
293 his response was more highly correlated with MCMV control than all other immune cell features.
294 iously immune to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology,
295  implanted in mice perinatally infected with MCMV versus controls.
296 s abolished in IL-12(-/-) mice infected with MCMV, whereas NK cells were still activated.
297 cted by infecting 22,000 G3 mutant mice with MCMV at an inoculum easily contained by WT animals.
298                  Upon infection of mice with MCMV mutants encoding Ag that can either be well or hard
299 and replication deficient adenovirus without MCMV inserts).
300 e and extent of aggregation with and without MCMV.

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