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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
16 operly through TLR3, TLR7 and TLR9, to acute MCMV infection to determine whether liver antiviral defe
18 oid and nonlymphoid tissues for months after MCMV infection, IL-12 receptor-deficient NK cells failed
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
33 on complete loss of genome replication of an MCMV mutant carrying a deletion of the ie3-specific exon
35 transcripts prompted the construction of an MCMV mutant lacking ie611 but retaining the coding capac
38 of MCMV infection, the infectious dose, and MCMV gene expression but was independent of IFNAR1, IL-1
40 nfection allows presentation of SIINFEKL and MCMV-derived Ags by different cells within the same anim
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
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
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
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
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
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
69 ry inflation, first described in murine CMV (MCMV) infection, is characterized by the accumulation of
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
76 toma, we assessed the effects of murine CMV (MCMV) perinatal infection in a GFAP-cre; Nf1(loxP/+); Tr
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
87 beyond their recognized role in controlling MCMV replication, NK cells preserve organ integrity and
89 f deletion mutants of mouse cytomegalovirus (MCMV) a mutant was identified that did not elicit cell r
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
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
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
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
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
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
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
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
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
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
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
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
165 protein allowed differentiation of MCMV from MCMV bound by antibody from the collision frequency decr
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
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
176 mPR expression and viral growth was found in MCMV-infected cells treated with Salmonella carrying the
178 ication in spleen and liver were observed in MCMV-infected Ebi3(-/-) and wild-type (WT) B6 mice.
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
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
188 ne to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology, enhanced vi
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
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
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
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
208 e responses to H-2(d)-restricted epitopes of MCMV pp89 and M18 Ags characteristic of infection with o
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
215 will be useful in elucidating mechanisms of MCMV reactivation, including the roles of injury and of
218 cytokine response during the early phase of MCMV infection in CD70(-/-) mice was paralleled by a red
223 nique domain, resulting from the splicing of MCMV ORFs m131 and m129 MCK-2 is essential for full MCMV
225 CD4 T cells that recognize them to fight off MCMV infection, and show that we can use the epitopes to
228 ary glands via Wharton's duct with tcMCMV or MCMV proteins focused to the salivary gland via replicat
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
235 vaccination of immunocompetent mice reduced MCMV replication in the same organs where CD4 cytotoxic
237 ticipate simultaneously during MAIDS-related MCMV retinitis, and all may play a role during AIDS-rela
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
243 sequence, we show that some of the long-term MCMV-immune mice mount a robust CD8 T cell cross-reactiv
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
255 After a transient phase of activation, the MCMV M45 protein blocks all canonical NF-kappaB-activati
257 th receptor activation and suppressed by the MCMV-encoded viral inhibitor of RIP activation (vIRA).
259 nd oral lavage was strongly decreased in the MCMV-infected Ebi3(-/-) B6 mice, suggesting that EBI3 pl
265 ayed shared genetic programs, validating the MCMV model for studies of CMV-specific T cells in vivo.
268 a glycoprotein-specific primary antibody to MCMV, and polystyrene bead "anchors," which were functio
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
276 defects in expansion during the response to MCMV infection, suggesting that their regulation by miR-
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
284 actin cytoskeleton observed after wild-type MCMV infection, and isolated expression of the M25 prote
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
294 iously immune to LCMV and then infected with MCMV (LCMV+MCMV), they had more severe immunopathology,
297 cted by infecting 22,000 G3 mutant mice with MCMV at an inoculum easily contained by WT animals.
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