ライフサイエンスコーパス: Sendai virus

1 le effect on the entry and egress of progeny Sendai virus.

2 d by a secondary (homologous) infection with Sendai virus.

3 e on the hemagglutinin-neuraminidase (HN) of Sendai virus.

4 ction from a challenge with a lethal dose of Sendai virus.

5 position from that previously identified for Sendai virus.

6 t failed to inhibit the IFN-alpha induced by Sendai virus.

7 o those induced by intranasal infection with Sendai virus.

8 ecreted IFN-alpha in response to HSV but not Sendai virus.

9 not to cells infected with vaccinia virus or Sendai virus.

10 syncytial virus, parainfluenza virus 5, and Sendai virus.

11 itic cells using a nonintegrating RNA virus, Sendai virus.

12 deficient or control mice were infected with Sendai virus.

13 llows: La Crosse virus, West Nile virus, and Sendai virus.

14 and non-expressing mouse cells infected with Sendai virus.

15 encephalitis virus, parainfluenza virus and Sendai virus.

16 t, and perforin-deficient mice infected with Sendai virus.

17 in cells infected with influenza A virus or Sendai virus.

18 nificantly lower than in cells infected with Sendai virus.

19 kappaB-dependent gene induction by dsRNA and Sendai virus.

20 a promoter activity following challenge with Sendai virus.

21 sion was strongly induced by IFN, dsRNA, and Sendai virus.

22 ally expressed unphosphorylated P protein of Sendai virus, a mouse parainfluenza virus, we have shown

23 (MDA5) sustains the acute immune response to Sendai virus, a mouse pathogen that causes chronic lung

24 e-associated phosphoprotein (P protein) from Sendai virus, a murine Paramyxovirus, is reported in the

25 Experiments in the 1960s showed that Sendai virus, a paramyxovirus, fused its membrane with t

26 llowing infection with the Cantell strain of Sendai virus, a potent inducer of IFN and cellular antiv

27 inoculated mice by the intranasal route with Sendai virus and conducted single-cell-sequencing analys

28 different stimuli, including infection with Sendai virus and liposome-mediated DNA transfection.

29 o induce detectable NF-kappaB activity, both Sendai virus and Newcastle disease virus infection led t

30 ulating type 1 IFN expression in response to Sendai virus and Newcastle disease virus infection.

31 G-I expression impaired only the response to Sendai virus and not extracellular poly(I-C).

32 ersistent infection by other viruses such as Sendai virus and reovirus.

33 ecific for influenza virus, as inhibition of Sendai virus and respiratory syncytial virus is not obse

34 ditionally replicative adenoviruses (CRAds), Sendai virus and respiratory syncytial virus.

35 egrating retroviral vectors, non-integrating Sendai virus and synthetic mRNAs.

36 Comparative studies of RSV and Sendai virus and the use of IFN-negative Vero cells indi

37 response to the TLR7 agonists imiquimod and Sendai virus and to the TLR9 agonist CpG.

38 e RNA viruses vesicular stomatitis virus and Sendai virus and to transfection with poly(I.C).

39 A intermediates, Newcastle disease virus and Sendai virus, and a DNA virus, herpes simplex virus type

40 e malaria parasite Plasmodium falciparum and Sendai virus, and along with the anion transporter, band

41 erologous HN/H proteins from simian virus 5, Sendai virus, and measles virus in coexpression experime

42 Approaches based on episomal DNA, Sendai virus, and messenger RNA (mRNA) can generate "foo

43 s of IFN-beta expression including Listeria, Sendai virus, and transfected dsRNA and dsDNA, further i

44 phosphorylation sites of the P protein from Sendai virus are localized by a direct approach using ma

45 f hemagglutinating virus of Japan (HVJ; also Sendai virus) are complexed with liposomes that encapsul

46 Using Sendai virus as a mouse model of respiratory virus infec

47 led accurately by direct i.n. inoculation of Sendai virus at a low dose and low volume and was comple

48 h before, or 2 h poststimulation with HSV or Sendai virus, but not when added 4 h postinduction.

49 The results of this study indicate that 1) Sendai virus can directly up-regulate TNF-alpha mRNA and

50 from infection with Newcastle disease virus, Sendai virus, canine distemper virus, and influenza A vi

51 ective-interfering (DI) particles present in Sendai virus-Cantell stocks are required for its robust

52 envelope protein and then challenged with a Sendai virus carrying a homologous HIV-1 envelope gene.

53 crophage accumulation in vivo, we contrasted Sendai virus-driven airway inflammation in wild-type and

54 gle-strand RNA (ssRNA) replication of RSVand Sendai virus, due to decreased expression and secretion

55 The nucleocapsid protein (NP) of Sendai virus encapsidates the genome RNA, forming a heli

56 Sendai virus encodes an RNA-dependent RNA polymerase whi

57 The polycistronic P/C mRNA of Sendai virus encodes five proteins (C', P, C, Y1, and Y2

58 s specific for both dominant and subdominant Sendai virus epitopes persisted for many weeks after pri

59 ith most paramyxoviruses, fusion mediated by Sendai virus F protein (F(SeV)) requires coexpression of

60 nal changes are regulated, we mutated in the Sendai virus F protein a highly conserved 10-residue seq

61 ation, we created chimeric mutants of M2 and Sendai virus F proteins, exchanging corresponding extrac

62 essed alone or coexpressed with heterologous Sendai virus F was totally TX-100 soluble but the membra

63 in a transient transfection production of a Sendai virus F/HN-pseudotyped HIV-1-based third generati

64 Two recombinant Sendai viruses, F-L179V and F-K180Q, were generated that

65 e immunized p53 mutant mice with peptides of Sendai virus (FAPGNYPAL) and influenza virus (ASNENMETM)

66 Because the use of concentrated Sendai virus for cell fusion induced an increase in intr

67 c galactose-terminated F-glycoprotein of the Sendai virus (FPL) for targeted delivery to hepatocytes.

68 had minimal effect on fusion directed by the Sendai virus glycoproteins.

69 nd knowing that the C protein of the related Sendai virus has particle assembly and infectivity facto

70 ovalently attached peptide sequence from the Sendai virus hemagglutinin/neuraminidase gene, have been

71 his study, we report that simian virus 5 and Sendai virus heterologous HN proteins and measles virus

72 However, when PBMC were induced with Sendai virus, IFN-alpha production was also reduced by I

73 Furthermore, FcgammaRIIB was required for Sendai virus immune complex uptake by splenic pDCs in vi

74 premature oocyte activation, we used diluted Sendai virus in calcium-free medium.

75 ere observed following a primary response to Sendai virus in IL-15(-/-) animals.

76 ed the pathogenesis of influenza A virus and Sendai virus in ISG15(-/-) mice.

77 n of the F protein modulate the virulence of Sendai virus in mice by influencing both the spread and

78 ivating stimuli, such as CpG, imiquimod, and Sendai virus, induced the most Tim-3 expression and subs

79 wn to block, via the NS3/4A serine protease, Sendai virus-induced activation of interferon regulatory

80 We demonstrate that VP35 blocks the Sendai virus-induced activation of two promoters which c

81 DPPI and neutrophils play a critical role in Sendai virus-induced asthma phenotype as a result of a D

82 he most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-beta mRNA accumulati

83 demonstrated that PKR was not necessary for Sendai virus-induced IFN synthesis, suggesting that PKR

84 in the steady state levels of both HSV- and Sendai virus-induced IFN-alpha1, -alpha2, and -beta mRNA

85 ooperatively repress IFN-alpha activation in Sendai virus-infected cells.

86 s IFN-lambda4 protein was detectable only in Sendai virus-infected PHHs from individuals with the dG

87 noclonal antibodies (mAbs) accumulate within Sendai virus-infected polarized cell monolayers and colo

88 induced by interferon, dsRNA treatments, or Sendai virus infection and acts as a feedback inhibitor

89 e capable of migrating to the lung following Sendai virus infection and express potent cytotoxic acti

90 er time for the development of TCE following Sendai virus infection and found a progressive increase

91 dentify virus-specific CD4(+) T cells during Sendai virus infection and the establishment of peripher

92 Here we show that control of a Sendai virus infection by primed CD4(+) T cells is media

93 knockdown of La in HEK 293 T cells increased Sendai virus infection efficiency, decreased IFN-beta, I

94 merate APCs during the course of respiratory Sendai virus infection in mice.

95 ic for subdominant epitopes can be primed by Sendai virus infection in the absence of a detectable ef

96 ene did not obviously modify the severity of Sendai virus infection in the highly susceptible 129/J m

97 IFN whereas MDA5 expression is increased by Sendai virus infection independently of signaling mediat

98 served that, although double-stranded RNA or Sendai virus infection induced the two genes with simila

99 Taken together, these data demonstrate that Sendai virus infection induces high frequencies of memor

100 but not isotype control, followed by murine Sendai virus infection led to development of Abs against

101 tissues and airways for several months after Sendai virus infection of C57BL/6 mice.

102 dominant and subdominant epitopes following Sendai virus infection of C57BL/6 mice.

103 Sendai virus infection of human trophectoderm progenitor

104 Subsequent Sendai virus infection of primed mice resulted in 1) a s

105 although they were robustly expressed after Sendai virus infection or dsRNA transfection.

106 he activation of the IFN-beta promoter after Sendai virus infection or poly(I.C) treatment.

107 We find that during Sendai virus infection this phenotype results from DVGs

108 I-C), both cell types signal the presence of Sendai virus infection through a TLR3-independent intrac

109 rate that host type I interferon response to Sendai virus infection was normal in NLRX1-silenced huma

110 he virus-activated factor (VAF) complex upon Sendai virus infection, bind to the IRF7 ISRE and IRFE a

111 blocked the induction of IFN-beta following Sendai virus infection, demonstrating that IE86's abilit

112 ated the subsequent effector CTL response to Sendai virus infection, demonstrating that memory CTLp p

113 ant epitopes is functional in the context of Sendai virus infection, memory CTLp specific for a subdo

114 Following intranasal Sendai virus infection, NP(324-332)/Kb-specific CTL domi

115 e was introduced into LLC-MK2 cells prior to Sendai virus infection, production of progeny virus was

116 duced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflamm

117 d binding of VAF are clearly increased after Sendai virus infection.

118 for suppressing IRF-3 activation induced by Sendai virus infection.

119 d proinflammatory chemokines during HCMV and Sendai virus infection.

120 airways following the resolution of a murine Sendai virus infection.

121 l months after recovery from an influenza or Sendai virus infection.

122 otential of CD8(+) memory T cells induced by Sendai virus infection.

123 bits the induction of IFNbeta mRNA following Sendai virus infection.

124 s the case for memory CTLp induction by live Sendai virus infection.

125 omponent of the effector response to primary Sendai virus infection.

126 es in miRNA abundance were identified during Sendai virus infection.

127 randed RNA, bacterial lipopolysaccaride, and Sendai virus infection.

128 accompanies the asthma phenotype induced by Sendai virus infection.

129 pha/beta-mediated luciferase expression upon Sendai virus infection.

130 Parainfluenza type 1 (Sendai) virus infection in young rats induces airway gro

131 n observed in animal models of influenza and sendai virus infections, as well as in patients infected

132 re more susceptible to influenza A virus and Sendai virus infections, ISGylation does not appear to m

133 ed by both Newcastle disease virus (NDV) and Sendai virus infections, without targeting it for protea

134 Sendai virus is eliminated from the respiratory tract of

135 rats by infection with parainfluenza type I (Sendai) virus is associated with bronchiolar fibrosis.

136 replaced with the corresponding residues of Sendai virus L protein failed to both transcribe the min

137 cids within this domain by the corresponding Sendai virus L protein residues yielded mutants with var

138 on with Encephalomyocarditis virus (EMCV) or Sendai virus led to higher levels of autophagy in wild-t

139 myelomonocytic cell line, NSP1beta inhibited Sendai virus-mediated activation of porcine IFN-beta pro

140 ot inhibit LMP1 induced NF-kappaB or TBK1 or Sendai virus-mediated IFN stimulated response element ac

141 we addressed these two issues using a murine Sendai virus model.

142 The Sendai virus mouse model was used to investigate the phe

143 onse to herpes simplex virus type-1 (HSV-1), Sendai virus, Newcastle disease virus, and vesicular sto

144 ent with this activity, DNA vaccination with Sendai virus NP induced a substantial degree of Ab-indep

145 A single peptide derived from the Sendai virus nucleoprotein (NP(324-332)) binds to both H

146 he induction of CD8+ memory CTL responses to Sendai virus nucleoprotein (NP) in C57BL/6 mice followin

147 interaction between the disordered domain of Sendai virus nucleoprotein (NT) and the C-terminal domai

148 A similar influx of nonproliferating Sendai virus nucleoprotein 324-332/K(b)-specific CD8(+)

149 show a transient increase in the numbers of Sendai virus nucleoprotein 324-332/K(b)-specific CD8(+)

150 tein, and on Kb of FAPGNYPAL, a peptide from Sendai virus nucleoprotein, was blocked by the proteasom

151 IFN-alpha production to Sendai virus occurs predominantly by monocytes, whereas

152 ize the effect of respiratory infection with Sendai virus on the number of Substance P/Neurokinin A-c

153 f IRF3 following treatment with HCMV but not Sendai virus or double-stranded RNA.

154 viruses in cell culture but does not inhibit Sendai virus or human metapneumovirus, two paramyxovirus

155 ection, because infection of host cells with Sendai virus or their exposure to supernatant from virus

156 e IFN-alpha in response to HSV-1, but not to Sendai virus or to Newcastle disease virus.

157 and IFNbeta secretion in MEFs infected with Sendai virus or transfected with poly(I:C).

158 otein 60 (Hsp60) in influenza virus- but not Sendai virus- or vaccinia virus-infected cells.

159 he C-terminal domain of the nucleoprotein of Sendai virus, over a large range of temperatures (268-29

160 se data indicate that phosphorylation of the Sendai virus P protein by PKC zeta plays a critical role

161 The Sendai virus P protein is an essential component of the

162 ireplicon and interact with HPIV 3 P and the Sendai virus P protein.

163 The Sendai virus P-L polymerase complex binds the NP-encapsi

164 ation of each alpha-helix in the tetramer of Sendai virus POD, this represents a novel orientation of

165 The Sendai virus polycistronic P/C mRNA encodes the P and C

166 herpes simplex virus (HSV) and HIV, whereas Sendai virus predominantly stimulates IFN-alpha producti

167 Uncoating of intact Sendai virus proceeds differently from uncoating describ

168 that the common procedure then used to grow Sendai virus produced damaged, pleomorphic virions.

169 ry properties, and the RIG-I affinity of the Sendai virus produced DI RNA both in vitro and in vivo.

170 se against RNA viruses such as influenza and Sendai virus, recognition of self-RNA by TLR7 also has b

171 vaccine (VV-sv) comprises CTL epitopes from Sendai virus, respiratory syncytial virus, and lymphocyt

172 Third, infection of LAG-3(-/-) mice with Sendai virus resulted in increased numbers of memory CD4

173 Recombinant Sendai virus (rSeV) was used as a live, attenuated vacci

174 We now describe recombinant Sendai viruses (rSeV) that express mutant F proteins con

175 bers of the Mononegavirales, we examined the Sendai virus (SeV) (family Paramyxoviridae) L protein by

176 Here, we investigated the minimum number of Sendai virus (SeV) and human cytomegalovirus (HCMV) part

177 Sendai virus (SeV) and human parainfluenza virus type 1

178 in cells capable of a strong IFN response to Sendai virus (SeV) and poly(I.C), NV RNA replicates effi

179 We have recently developed recombinant Sendai virus (SeV) as a new gene transfer agent.

180 ainfluenza virus (hPIV) type 1, 2, and 3 and Sendai virus (SeV) HN proteins.

181 ly after in vivo and in vitro infection with Sendai virus (SeV) in the absence of TLR3, 7, 8, or 9 si

182 infected with 2 different concentrations of Sendai virus (SeV) induce 2 distinct type I IFN subtype

183 Sendai virus (SeV) infection causes apoptosis, which is

184 Sendai virus (SeV) infection causes the transcriptional

185 ck the accumulation of IFN-beta triggered by Sendai virus (SeV) infection.

186 on with a mouse parainfluenza virus known as Sendai virus (SeV) leads to long-term activation of inna

187 ignaling, including RIG-I activators such as Sendai virus (SeV) or 5'-triphosphate RNA, or MDA5 activ

188 Infection of several human cell lines with Sendai virus (SeV) or human parainfluenza virus 3, two p

189 ion of cellular origin (hESC vs. hiPSC), the Sendai virus (SeV) reprogramming method and genetic back

190 Here, we show that Sendai virus (SeV) vectors expressing cardiac reprogramm

191 s (Cantell and 52) of the murine respiratory Sendai virus (SeV) with differential abilities to induce

192 members of the paramyxoviridae such as PIV3, Sendai virus (SeV), and canine distemper virus (CDV) are

193 N response to Newcastle disease virus (NDV), Sendai virus (SeV), and Semliki Forest virus (SFV) infec

194 hen IRF-3-knockdown cells were infected with Sendai virus (SeV), persistent infection (PI) was establ

195 is virus, Newcastle disease virus (NDV), and Sendai virus (SeV), was significantly inhibited in L2 ce

196 Induction of apoptosis in cells infected by Sendai virus (SeV), which triggers the cytosolic RIG-I p

197 an cells, including primary cells, inhibited Sendai virus (SeV)-mediated IFN induction and enhanced v

198 either TNF-alpha treatment or infection with Sendai virus (SeV).

199 from pathogenesis caused by the respirovirus Sendai virus (SeV).

200 Rs (CpG-A ODN signaling via TLR9, or R837 or Sendai virus signaling via TLR7) and MyD88-independent r

201 Upon infection with Sendai virus, SINTBAD is essential for the efficient ind

202 teins between two different paramyxoviruses, Sendai virus (SN) and human parainfluenza virus type 3 (

203 ype 1 (PI1), type 2 (PI2), and type 3 (PI3), Sendai virus (SN), and simian virus 5 (SV5) by expressio

204 The development and persistence of Sendai virus-specific CD4+ T cell memory has been analyz

205 a heterologous influenza virus infection on Sendai virus-specific CD8(+) effector/memory cells prese

206 MDA5-deficient DCs respond inefficiently to Sendai virus stocks containing DI particles; 3) DI parti

207 Sendai virus strain Cantell has a particularly strong ab

208 e defective interfering (DI) RNA produced by Sendai virus strain Cantell.

209 Here we describe a recombinant Sendai virus strategy for probing the effector role(s) o

210 Sendai virus (SV) and human parainfluenza virus type 1 (

211 n TM domains from two other paramyxoviruses, Sendai virus (SV) and measles virus (MV), or the TM doma

212 Intranasal deposition of Sendai virus (SV) in C57BL/6 mice provokes an Ab-forming

213 We investigated the roles of three Sendai virus (SV) membrane proteins in the production of

214 transiently transfecting HN cDNA genes into Sendai virus (SV)-infected cells.

215 de (LPS), double-stranded RNA (poly(I-C)) or Sendai virus (SV).

216 human parainfluenza virus type 1 (hPIV1) and Sendai virus (SV).

217 used the murine parainfluenza virus type 1 (Sendai virus [SV]) as a xenogeneic vector to deliver the

218 Here, we used luciferase-expressing reporter Sendai viruses (the murine counterpart of HPIV1) to noni

219 al innate immune receptor ligands, including Sendai virus, the dsRNA mimetic polyinosinic-polycytidyl

220 When challenged with Sendai virus, the IFN response was normal in TBK1(-/-) m

221 myxoviral respiratory infection triggered by Sendai virus to examine the response of conventional and

222 h recombinant type III IFNs or infected with Sendai virus to model acute viral infection and subseque

223 Here we use a common mouse paramyxovirus (Sendai virus) to show that a prominent early event in re

224 virus-induced chronic lung disease, in which Sendai virus triggered a switch to persistent mucous cel

225 ide, but did not induce Abs specific for the Sendai virus virion.

226 st, IFN-beta responses to the RIG-I-detected Sendai virus were diminished, suggesting that TRIM13 may

227 Both nonattenuated and attenuated reporter Sendai viruses were used, and three inoculation strategi

228 row were still susceptible to infection with Sendai virus, whereas wild-type mice that received Stat1

229 from influenza virus, but not C protein from Sendai virus, which does not bind dsRNA, likewise effect

230 In contrast, the envelope of Sendai virus, which is derived from cytoplasmic membrane

231 etected only in cells infected with NDV, not Sendai virus, while both viruses activate IRF-3 and IRF-

232 element (ISRE) promoter after infection with Sendai virus, while only ORF 3b and ORF 6 proteins were

233 ice from lethal infection with a recombinant Sendai virus whose HN was replaced with that of hPIV-1 (

234 sion assay was made during the fusion of the Sendai virus with erythrocyte ghosts.