ライフサイエンスコーパス: EMCV

1 EMCV 30/87-infected macaques remained overtly asymptomat

2 EMCV antigens and RNA were demonstrated in the myocardiu

3 EMCV infection also activates the mitogen-activated prot

4 EMCV initiation does not involve scanning and does not r

5 EMCV persisted at higher levels in CD1d-knockout (KO) sp

6 EMCV-induced macrophage activation has been shown to req

7 nverting enzyme; and demonstration of active EMCV transcription by reverse transcription-PCR.

8 t mice (lacking all NKT cells) against acute EMCV infection was further studied in vitro and in vivo.

9 e apoptosis, and cleavage of caspase 3 after EMCV infection were attenuated in alphaMHC-MDA5 mice.

10 e protective actions of nitric oxide against EMCV infection are selective for beta-cells and associat

11 e, alphaMHC-MDA5 mice were protected against EMCV-induced myocardial dysfunction.

12 The optimal innate immune response against EMCV in vivo requires CD1d.

13 irus 2A(pro) gene to the EMCV genome allowed EMCV to replicate in IFN-alpha-pretreated cells.

14 Although EMCV is sensitive to IFN-alpha, coinfection of cells wit

15 er capped reporter RNA, an RNA containing an EMCV internal ribosomal entry site (IRES) or an RNA with

16 Analysis of the nucleotide sequence of an EMCV strain isolated from an aborted swine fetus (EMCV 3

17 t all p50 knockout (p50 -/-) mice survive an EMCV infection that readily kills normal mice.

18 Furthermore, dsRNA and EMCV stimulate COX-2 expression and PGE(2) accumulation

19 ERK inhibition does not modulate dsRNA- and EMCV-induced COX-2 expression and PGE2 production by mac

20 AW 264.7 cells fails to attenuate dsRNA- and EMCV-induced COX-2 expression or PGE(2) production.

21 ibitor bromoenol lactone prevents dsRNA- and EMCV-stimulated inducible NO synthase expression; howeve

22 ha, coinfection of cells with poliovirus and EMCV leads to EMCV replication in IFN-alpha-pretreated c

23 t nitric oxide inhibits EMCV replication and EMCV-mediated beta-cell lysis and that this protection i

24 RNase L induction markedly enhanced the anti-EMCV activity of IFN via a reduction in EMCV RNA.

25 the combination of NK and NKT cells to anti-EMCV responses and that none of these cell types was the

26 itors of mitochondrial respiration attenuate EMCV replication in beta-cells, and this inhibition is a

27 itochondrial oxidative metabolism attenuates EMCV-mediated beta-cell lysis by inhibiting viral replic

28 n of cellular ATP, NO selectively attenuates EMCV replication in, and lysis of, beta-cells.

29 rophages as a result of interactions between EMCV capsid proteins and cell surface receptors.

30 and Renilla luciferase [rl]) placed between EMCV IRES and SIRES segments.

31 o different PI3K regulated pathways to block EMCV- and HSV-induced cell death.

32 the absence of p53, the replication of both EMCV and HPIV3 was retarded, whereas, conversely, VSV re

33 rulent, serotypically identical cardiovirus, EMCV.

34 ncoding luciferase, followed by the complete EMCV IRES fused to the P2-P3 region of the poliovirus ge

35 TLR3 and MDA5 controlled EMCV-D infection and diabetes by acting in hematopoietic

36 ed with encephalomyocarditis virus strain D (EMCV-D), which has tropism for the insulin-producing bet

37 emical inhibitors of TNK2 and WASL decreased EMCV infection.

38 ability of the NLRP3 inflammasome to detect EMCV and VSV, wild-type and caspase-1-deficient mice wer

39 ly important in suppressing apoptosis during EMCV infection.

40 tions nonredundantly to modulate MDA5 during EMCV infection.

41 The activation of mTORC1 during EMCV infection is CCR5-dependent and appears to function

42 Consistent with this hypothesis, empty EMCV capsids induced comparable levels of iNOS expressio

43 either Coxsackie (CV), encephalomyocarditis (EMCV), influenza A (IAV), measles (MV), Sendai (SV), or

44 SIRES) in place of the encephalomyocarditis (EMCV) IRES in mediating downstream reporter gene express

45 strain isolated from an aborted swine fetus (EMCV 30/87) revealed that the virus had a poly(C) tract

46 Finally, EMCV infection in vivo produced higher levels of viremia

47 conferred resistance to infection with FMDV, EMCV, TMEV, and equine rhinitis A virus (ERAV).

48 f 100 commercial pigs that were negative for EMCV antibodies identified two pig hearts positive for E

49 odies identified two pig hearts positive for EMCV RNA.

50 n of apoptosis by NF-kappaB1 is required for EMCV virulence in vivo.

51 etic evidence that iPLA2beta is required for EMCV-induced iNOS expression.

52 pendent protein kinase R is not required for EMCV-stimulated COX-2 expression, suggesting the presenc

53 ow that the presence of Ccr5 is required for EMCV-stimulated mitogen-activated protein (MAP) kinase a

54 ing using a monoclonal antibody specific for EMCV RNA polymerase, which is expressed only in producti

55 trast, the luciferase activity detected from EMCV-Luc-PV increased for approximately 12 h following t

56 La cell nuclei treated with L, or those from EMCV-infected cells, showed reproducibly altered pattern

57 Expression of a functional EMCV 3C proteinase was necessary and sufficient to stimu

58 A second dicistronic genome, EMCV-Luc-PV, was constructed with the first 108 nucleoti

59 we reconstituted it in vitro on beta-globin, EMCV IRES, and CrPV IRES mRNAs that use unrelated initia

60 tein synthesis was not detectably altered in EMCV-infected cells expressing a cleavage-resistant PABP

61 ted in a delay in virus-induced apoptosis in EMCV-infected U937 cells, allowing the eventual establis

62 t cells demonstrating that TNK2 functions in EMCV entry.

63 ficient to block Nup hyperphosphorylation in EMCV-infected or L-expressing cells.

64 anti-EMCV activity of IFN via a reduction in EMCV RNA.

65 versely, genomic deletion of the L region in EMCV generates viruses that are less potent at stimulati

66 The short poly(C) tract in EMCV 30/87 (CUC(5)UC(8)) was comparable to that of strai

67 f 2-5A, was not observed in RNase L-induced, EMCV-infected cells; however, transfection of 2-5A into

68 xpression, (S)-BEL more effectively inhibits EMCV-induced CREB phosphorylation than (R)-BEL in macrop

69 show that one mechanism by which NO inhibits EMCV replication is by attenuating the accumulation of p

70 ve recently shown that nitric oxide inhibits EMCV replication and EMCV-mediated beta-cell lysis and t

71 py studies showing presence of intracellular EMCV virions and chromatin condensation; detection of vi

72 lymphocytes confer protection against lethal EMCV in the absence of prophylactic antibodies, suggests

73 tion of CD8(+) T lymphocytes prior to lethal EMCV challenge ablated protection in vMC24-immunized RHA

74 s against virally mediated lysis by limiting EMCV replication.

75 The luciferase activity detected from PV-Luc-EMCV increased rapidly during the first 4 h following tr

76 The PV-Luc-EMCV replicon was unstable upon serial passage in the pr

77 2-P3 region of the poliovirus genome (PV-Luc-EMCV).

78 rase activity were similar to that of PV-Luc-EMCV.

79 of mitochondrial metabolism does not modify EMCV replication or decrease ATP levels.

80 ate with PKR activity or the accumulation of EMCV RNA, suggesting that an interaction between a struc

81 on of antiviral cytokines and-in the case of EMCV and HSV-1-reduced survival.

82 the effect of ITAFs on the conformations of EMCV and FMDV IRESs by comparing their influence on hydr

83 is not required for the replication cycle of EMCV.

84 more, optimal resistance to repeat cycles of EMCV infection in vitro was also shown to depend on CD1d

85 splenocytes exhibited in vitro cytolysis of EMCV-infected targets.

86 The encapsidation of EMCV-Luc-PV was compared to that of monocistronic replic

87 TORC1 inhibition increases the expression of EMCV polymerase.

88 -alpha synthesis, whereas the infectivity of EMCV was drastically attenuated.

89 Mechanistically, reduced internalization of EMCV was observed in TNK2 deficient cells demonstrating

90 Furthermore, the level of EMCV replication in wild-type splenocytes was markedly a

91 Sixteen percent of EMCV 30/87-infected pigs developed acute fatal cardiac f

92 mice infected with >/==" BORDER="0">4 PFU of EMCV 30/87 developed acute encephalitis that resulted in

93 RNase L induction reduced the rate of EMCV RNA synthesis, suggesting that RNase L may target v

94 Thus, the L region antisense RNA of EMCV is a key determinant of innate immunity to the viru

95 kine receptor, in transducing the signals of EMCV infection that result in the expression of inflamma

96 omoenol lactone does not attenuate dsRNA- or EMCV-induced COX-2 expression by macrophages.

97 of either kinase fails to prevent dsRNA- or EMCV-stimulated inducible NO synthase expression by macr

98 oding luciferase with either a poliovirus or EMCV IRES.

99 old shorter than the poly(C) tracts of other EMCV strains and 4-fold shorter than that of Mengo virus

100 ing the eventual establishment of persistent EMCV infection in these cells (U9K-AV2).

101 Porcine EMCV productively infected primary human cardiomyocytes

102 The findings that porcine EMCV can persist in pig myocardium and can infect human

103 n platelet count and increased survival post EMCV infection.

104 We now report that recombinant EMCV L triggers the unregulated efflux of protein cargo

105 Reduced EMCV lethality was observed in mice lacking TNK2.

106 alomyocarditis virus 5'-untranslated region (EMCV-UTR) for cap-independent translation in mammalian c

107 monstrate that PABP cleavage by 3C regulates EMCV replication.

108 We show that PI3K regulates EMCV-stimulated iNOS and COX-2 expression by two indepen

109 Repeated EMCV infection in vitro induced less IFN-gamma and alpha

110 e in the early control of virus replication: EMCV mRNA accumulates to sevenfold higher levels in Ccr5

111 In agreement with previous reports, EMCV induced a marked decrease in host mRNA translation.

112 and cynomolgus macaques resulted in similar EMCV 30/87 pathogenesis, with the heart and brain as the

113 Initiation on some EMCV-like IRESs requires additional noncanonical initiat

114 be 4- and 8-fold higher, respectively, than EMCV IRES.

115 Here, we establish that EMCV infection stimulates site-specific PABP proteolysis

116 xamination of this cell death, we found that EMCV infection induced both plasma membrane and nuclear

117 The EMCV IRES sequence was placed between the first and seco

118 ted evidence of genetic instability, and the EMCV IRES was deleted upon serial passage.

119 eIF4GI bound the EMCV IRES and beta-globin mRNA with similar affinities,

120 and from transfection of RNA containing the EMCV IRES downstream of the first 237 nt of HAV demonstr

121 carditis virus (EMCV) chimera containing the EMCV IRES element was not affected significantly in the

122 In contrast, the EMCV-Luc-PV replicon was genetically stable during passa

123 on with eIF4A increased its affinity for the EMCV IRES (but not beta-globin RNA) by 2 orders of magni

124 ly higher for the SIRES vectors than for the EMCV IRES vectors.

125 n, no minus-strand RNA was produced from the EMCV chimeric template RNA in vitro.

126 equence corresponding to the L region of the EMCV antisense RNA.

127 ts of eIF4F bind immediately upstream of the EMCV initiation codon and promote binding of 43S complex

128 the presence of VV-P1, with deletions of the EMCV IRES region detected even during the initial transf

129 d for four RNA oligonucleotides based on the EMCV IRES Domain I to assess the contributions of helix,

130 show that TMEV 2A trans-activates PRF on the EMCV signal but not vice versa.

131 upports efficient ribosomal recruitment: the EMCV IRES is stimulated by pyrimidine tract binding prot

132 nic poliovirus replicons by substituting the EMCV IRES and the gene encoding luciferase in place of t

133 Together, these results establish that the EMCV 3C proteinase mediates site-specific PABP cleavage

134 dition of the poliovirus 2A(pro) gene to the EMCV genome allowed EMCV to replicate in IFN-alpha-pretr

135 ed for specific high-affinity binding to the EMCV IRES and for internal ribosomal entry on this RNA.

136 otides of the poliovirus genome fused to the EMCV IRES, followed by the gene encoding luciferase and

137 tly than the monocistronic replicon with the EMCV IRES but less efficiently than the monicistronic re

138 al to or greater than that achieved with the EMCV IRES.

139 ty of p85alpha(-/-) embryonic fibroblasts to EMCV-induced cell death is specifically corrected by ove

140 n of cells with poliovirus and EMCV leads to EMCV replication in IFN-alpha-pretreated cells.

141 y role for Ccr5 in the antiviral response to EMCV in which this chemokine receptor participates in re

142 l induction of iNOS and COX-2 in response to EMCV infection by a mechanism that is independent of Akt

143 n of cyclooxygenase-2 (COX)-2 in response to EMCV infection was examined.

144 In response to EMCV infection, Akt is activated and regulates the trans

145 tivation and COX-2 expression in response to EMCV or poly(IC) does not require the presence the dsRNA

146 ing protein (MAVS) activation in response to EMCV RNA stimulation.

147 3K in regulating the macrophage responses to EMCV.

148 MDA5-knockout mice are highly susceptible to EMCV infection and develop significant myocardial injury

149 alphaMHC-MDA5 mice were less susceptible to EMCV infection and had a significantly lower cardiac vir

150 enza virus M2 or encephalomyocarditis virus (EMCV) 2B protein triggers translocation of mtDNA into th

151 Encephalomyocarditis virus (EMCV) and hepatitis C virus epitomize distinct mechanism

152 death induced by encephalomyocarditis virus (EMCV) and HSV.

153 ruses, including encephalomyocarditis virus (EMCV) and human parainfluenza virus type 3 (HPIV3), indu

154 virus 1 (HSV-1), encephalomyocarditis virus (EMCV) and influenza A virus (IAV), we identified several

155 using wild-type Encephalomyocarditis virus (EMCV) and Mengo virus, which have long poly(C) tracts (6

156 directed by the encephalomyocarditis virus (EMCV) and poliovirus IRESs in a cell-free system and in

157 free systems for encephalomyocarditis virus (EMCV) and Theiler's murine encephalomyelitis virus (TMEV

158 her RNA viruses, encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV), activate the

159 hown that L from encephalomyocarditis virus (EMCV) binds and inhibits the activity of Ran-GTPase, a k

160 lication of a PV-encephalomyocarditis virus (EMCV) chimera containing the EMCV IRES element was not a

161 te (IRES) of the encephalomyocarditis virus (EMCV) genomic RNA.

162 264.7 cells with encephalomyocarditis virus (EMCV) induces iNOS expression and nitric oxide productio

163 e studied murine encephalomyocarditis virus (EMCV) infection in mice and cell lines defective in NF-k

164 n against lethal encephalomyocarditis virus (EMCV) infection in the natural host.

165 igated following encephalomyocarditis virus (EMCV) infection of cell lines in which expression of tra

166 Encephalomyocarditis virus (EMCV) infection of macrophages results in the expression

167 imilar to dsRNA, encephalomyocarditis virus (EMCV) infection of RAW 264.7 cells stimulates COX-2 expr

168 n, the impact of encephalomyocarditis virus (EMCV) infection on the host poly(A)-binding protein (PAB

169 Highly cytolytic encephalomyocarditis virus (EMCV) infection was shifted to persistent infection as a

170 In response to encephalomyocarditis virus (EMCV) infection, resident islet macrophages release the

171 , eIF4A, and the encephalomyocarditis virus (EMCV) internal ribosomal entry site (IRES) and mediates

172 n (NCR) with the encephalomyocarditis virus (EMCV) internal ribosomal entry site, thereby deleting th

173 s containing the encephalomyocarditis virus (EMCV) internal ribosome entry segment (IRES) and various

174 As containing an encephalomyocarditis virus (EMCV) internal ribosome entry site (IRES) at the same si

175 by inserting an encephalomyocarditis virus (EMCV) internal ribosome entry site (IRES) between NS2 an

176 by inserting an encephalomyocarditis virus (EMCV) internal ribosome entry site (IRES) between these

177 insertion of the encephalomyocarditis virus (EMCV) IRES element between two open-reading frames of a

178 nt luciferase or encephalomyocarditis virus (EMCV) IRES luciferase reporter translation was observed.

179 active than the encephalomyocarditis virus (EMCV) IRES.

180 The encephalomyocarditis virus (EMCV) is a mouse-tropic member of the picornavirus famil

181 Encephalomyocarditis virus (EMCV) is a picornavirus that can cause paralysis, diabet

182 Encephalomyocarditis virus (EMCV) is capable of stimulating inflammatory gene expres

183 entry (IRES) for encephalomyocarditis virus (EMCV) is positioned between the P1 and P2-P3 open readin

184 d that -1 PRF in encephalomyocarditis virus (EMCV) is trans-activated by the viral 2A protein, leadin

185 ymes involved in encephalomyocarditis virus (EMCV) L-directed Nup phosphorylation were screened with

186 y of the porcine encephalomyocarditis virus (EMCV) model for such studies by determining its ability

187 tivators such as encephalomyocarditis virus (EMCV) or poly(I . C).

188 l infection with Encephalomyocarditis virus (EMCV) or Sendai virus led to higher levels of autophagy

189 r infection with encephalomyocarditis virus (EMCV) or West Nile virus.

190 t infection with encephalomyocarditis virus (EMCV) rapidly reduces platelet count, and this response

191 r (L) protein of encephalomyocarditis virus (EMCV) shuts off host cell nucleocytoplasmic trafficking

192 y site (IRES) of encephalomyocarditis virus (EMCV) which mediates initiation of cap-independent trans

193 ls infected with encephalomyocarditis virus (EMCV), a cardiovirus.

194 ls infected with encephalomyocarditis virus (EMCV), a picornavirus detected by MDA5 and LGP2 but not

195 Rhabdovirus, and encephalomyocarditis virus (EMCV), a picornavirus of the Cardiovirus genus, was comp

196 acellular dsRNA, encephalomyocarditis virus (EMCV), and herpes simplex virus 1 (HSV-1) show impaired

197 tis virus (VSV), Encephalomyocarditis virus (EMCV), and Reovirus-3 virus (Reo-3) in a STAT1-dependent

198 or NCK1 reduced encephalomyocarditis virus (EMCV), coxsackievirus B3 (CVB3), poliovirus and enterovi

199 sites (IRESs) of encephalomyocarditis virus (EMCV), foot-and-mouth disease virus (FMDV) and other pic

200 eric recombinant encephalomyocarditis virus (EMCV), in which we functionally replaced the endogenous

201 viruses, such as encephalomyocarditis virus (EMCV), induce a pro-inflammatory response in islets lead

202 novirus (Adeno), encephalomyocarditis virus (EMCV), influenza virus (H1N1) with different sizes.

203 virus (VSV) and encephalomyocarditis virus (EMCV), may also activate the same pathway.

204 For encephalomyocarditis virus (EMCV), the prototype of the genus Cardiovirus, these pro

205 l challenge with encephalomyocarditis virus (EMCV), which is sensed by MDA5, Trim13(-/-) mice produce

206 is required for encephalomyocarditis virus (EMCV)- and dsRNA-stimulated COX-2 expression in mouse ma

207 e susceptible to encephalomyocarditis virus (EMCV)-induced death and fail to mount a characteristic t

208 (S)-BEL inhibits encephalomyocarditis virus (EMCV)-induced iNOS expression, nitric oxide production,

209 (IRES) from the Encephalomyocarditis Virus (EMCV).

210 oV) OC43 but not encephalomyocarditis virus (EMCV).

211 athogens such as encephalomyocarditis virus (EMCV).

212 family, such as encephalomyocarditis virus (EMCV).

213 embryonic fibroblasts (MEFs) challenged with EMCV or poly(I .

214 -fold greater using SIRES when compared with EMCV IRES.

215 Fibroblasts infected with EMCV (or treated with dsRNA) produced interleukin-6, an

216 mice, the MDA5(K23R/K43R) mice infected with EMCV displayed increased myocardial injury and mortality

217 d that p50 -/- and p65 -/- MEF infected with EMCV undergo enhanced, premature cytotoxicity.

218 d transient hyperglycemia when infected with EMCV-D, whereas homozygous Mda5-/- mice developed severe

219 RAW-264.7 cells with dsRNA or infection with EMCV stimulates the rapid activation of the MAPKs p38, J

220 ritoneal inoculation of 5-week-old pigs with EMCV-30, a strain isolated from commercial pigs, resulte