ライフサイエンスコーパス: Sendai virus

1 spiratory infection with a natural pathogen (Sendai virus).

2 nificantly lower than in cells infected with Sendai virus.

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

4 a promoter activity following challenge with Sendai virus.

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

6 mes during infections with the paramyxovirus Sendai virus.

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

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

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

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

11 position from that previously identified for Sendai virus.

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

13 o those induced by intranasal infection with Sendai virus.

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

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

16 rogressive postviral lung disease due to the Sendai virus.

17 mortality to the murine parainfluenza virus Sendai virus.

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

19 nal factors Oct4, Sox2, Klf4 and c-Myc using Sendai virus.

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

21 deficient or control mice were infected with Sendai virus.

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

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

24 encephalitis virus, parainfluenza virus and Sendai virus.

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

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

27 VSV-DeltaM51 (but not of wild-type VSV) and Sendai virus (a paramyxovirus) via inhibition of antivir

28 r, G(2)/M arrest enhanced the replication of Sendai virus (a paramyxovirus), which is also highly sen

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

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

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

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

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

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

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

36 scriptional activity, efficiently suppressed Sendai virus and murine hepatitis virus replication.

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

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

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

40 IRF3-mediated IFN-beta expression induced by Sendai virus and poly(I:C).

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

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

43 7 inhibits the paramyxo-/pneumoviruses (e.g. Sendai virus and respiratory syncytial virus) by interfe

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

45 ctivator lipopolysaccharide or infected with Sendai virus and SAMHD1 reconstitution inhibited phospho

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

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

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

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

50 of infection because of mouse parainfluenza (Sendai) virus and human enterovirus D68 (EV-D68).

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

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

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

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

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

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

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

58 ontrol of innate immune signaling induced by Sendai virus argue against an active block of IRF3 activ

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

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

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

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

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

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

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

66 ive strategy, we have developed an RNA-based Sendai virus CRISPR-Cas9 delivery vector that does not i

67 system in mammalian cells using recombinant Sendai virus designed to be targeted by endogenous host

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

69 Sendai virus drives postviral airway disease in nonatopi

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

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

72 Sendai virus encodes an RNA-dependent RNA polymerase whi

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

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

75 eneration lentiviral vector pseudotyped with Sendai virus F and HN envelope proteins (rSIV.F/HN) has

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

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

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

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

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

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

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

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

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

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

86 e inoculation with a normally lethal dose of Sendai virus greatly reduced death.

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

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

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

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

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

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

93 s, we applied this pressure to a recombinant Sendai virus in cell culture.

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

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

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

97 ting atopy on postviral airway disease using Sendai virus in mice, which models RSV infection in huma

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

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

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

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

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

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

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

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

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

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

108 ed phosphorylation of IKKalpha/beta/gamma in Sendai virus-infected THP-1 cells.

109 Of note, in lipopolysaccharide-treated or Sendai virus-infected U937 or THP-1 cells, the mNLS vari

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

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

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

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

114 Sendai virus infection bestows mature AT2 cells with neo

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

116 In Irf3(-/-) mice, consequently, Sendai virus infection caused enhanced inflammation in t

117 tiparameter imaging of cellular responses to Sendai virus infection coupled with in situ cDNA sequenc

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

119 d suppressed MAVS aggregation in response to Sendai virus infection in human monocytic THP-1 cells.

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

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

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

123 response in lung epithelial cells following Sendai virus infection in vivo.

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

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

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

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

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

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

130 Sendai virus infection of human trophectoderm progenitor

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

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

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

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

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

136 the chronic lung disease that develops after Sendai virus infection was also increased in Foxj1-Scgb1

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

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

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

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

141 IFN and showed higher susceptibility during Sendai virus infection, demonstrating the importance of

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

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

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

145 s regarding the proviral role of OPTN during Sendai virus infection, we demonstrate that lack of OPTN

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

147 N-beta, and TNF-alpha mRNA levels induced by Sendai virus infection.

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

149 accompanies the asthma phenotype induced by Sendai virus infection.

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

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

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

153 d proinflammatory chemokines during HCMV and Sendai virus infection.

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

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

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

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

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

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

160 in the lung, as well as their changes after Sendai virus infection.

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

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

163 ective viral genomes (DVGs) generated during Sendai virus infections accumulate in the cytoplasm of s

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

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

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

167 ratory virus disease following influenza and Sendai virus infections.

168 Sendai virus is eliminated from the respiratory tract of

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

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

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

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

173 identified regulators of IRF3 translocation, Sendai virus localization, and peroxisomal biogenesis.

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

175 show that N(pro) is also able to antagonise Sendai virus-mediated apoptosis in PK-15 cells.

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

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

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

179 ete protection against lethal infection in a Sendai virus mouse surrogate model of human HPIV3 diseas

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

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

182 TRM, but we were unable to generate de novo Sendai virus NP+ CD8+ TRM following LAIV immunization in

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

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

185 also inserted a CD8+ T cell epitope from the Sendai virus nucleoprotein (NP) to assess both generatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 Uncoating of intact Sendai virus proceeds differently from uncoating describ

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

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

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

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

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

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

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

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

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

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

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

218 (MAVS) pathway and antiviral immunity during Sendai virus (SeV) and respiratory syncytial virus (RSV)

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

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

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

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

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

224 Sendai virus (SeV) infection causes the transcriptional

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

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

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

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

229 hronic lung disease caused by infection with Sendai virus (SeV) or influenza A virus in mice.

230 w that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-se

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

232 We analyzed the DRS outputs of multiple Sendai virus (SeV) stocks to highlight both the utility

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 Sendai virus strain Cantell has a particularly strong ab

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

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

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

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

255 hows an excellent antiviral activity against Sendai virus (SV) by inhibiting its entry to the cells.

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

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

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

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

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

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

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

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

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

265 measurements are possible by using reporter Sendai viruses, the murine counterpart of HPIV 1, that e

266 ession to target NP of influenza A virus and Sendai virus to ascertain how this would impact genomic

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

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

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

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

271 a temperature-sensitive and less immunogenic Sendai virus (ts SeV) as a novel delivery vector for CRI

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

273 ven extensive time, escape of miRNA-targeted Sendai virus was enabled by host adenosine deaminase act

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

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

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

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

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

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

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

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

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