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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 rulent, serotypically identical cardiovirus, EMCV.

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

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

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

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

33 ly important in suppressing apoptosis during EMCV infection.

34 tions nonredundantly to modulate MDA5 during EMCV infection.

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

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

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

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

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

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

41 odies identified two pig hearts positive for EMCV RNA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 2-P3 region of the poliovirus genome (PV-Luc-EMCV).

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

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

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

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

69 is not required for the replication cycle of EMCV.

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

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

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

73 TORC1 inhibition increases the expression of EMCV polymerase.

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

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

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

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

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

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

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

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

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

83 oding luciferase with either a poliovirus or EMCV IRES.

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

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

86 Porcine EMCV productively infected primary human cardiomyocytes

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

88 n platelet count and increased survival post EMCV infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 3K in regulating the macrophage responses to EMCV.

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

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

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

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

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

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

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

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

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

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

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

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

142 264.7 cells with encephalomyocarditis virus (EMCV) induces iNOS expression and nitric oxide productio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 active than the encephalomyocarditis virus (EMCV) IRES.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 athogens such as encephalomyocarditis virus (EMCV).

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

182 family, such as encephalomyocarditis virus (EMCV).

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

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

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

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

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

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

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