ライフサイエンスコーパス: measles virus

1 ly nuclear during infections with dengue and measles virus.

2 t were acutely or persistently infected with measles virus.

3 links into the prefusion F protein trimer of measles virus.

4 ikelihood of importation and transmission of measles virus.

5 ith inapparent measles virus infections shed measles virus.

6 ups of individuals who are not immune to the measles virus.

7 the avidity of antibodies were measured for measles virus.

8 ate of the X domain of phosphoprotein (P) of measles virus.

9 rization of currently circulating strains of measles viruses.

10 Measles virus, a member of the Morbillivirus family, inf

11 Our aim was to assess population immunity to measles virus after a mass vaccination campaign in a reg

12 rains of patients persistently infected with measles virus, although the precise role of ADAR during

13 d from children and tested for antibodies to measles virus and HIV-1 by EIA.

14 les is a highly contagious disease caused by measles virus and is one of the most devastating infecti

15 ous disease that results from infection with measles virus and is still responsible for more than 100

16 Using Moraten vaccine strain-derived measles virus and isogenic mutants deficient for either

17 nstrate that the last 50 amino acids of both measles virus and mumps virus P (measles virus P, 457 to

18 and LGP2 variants unable to be recognized by measles virus and parainfluenza virus 5 (PIV5) V protein

19 e are a large group of viruses that includes measles virus and parainfluenza viruses.

20 bers of the order Mononegavirales, including measles virus and rabies virus.

21 The V proteins of measles virus and the related paramyxovirus Nipah virus

22 679 children (67%) had antibodies to measles virus, and 64 (6%) children had antibodies to HI

23 virus, human parainfluenza virus type 3, and measles virus, and highly lethal emerging pathogens such

24 d residues in the V proteins of Nipah virus, measles virus, and mumps virus also abolishes MDA5 inter

25 gavirales, which also includes rabies virus, measles virus, and respiratory syncytial virus.

26 antiretroviral therapy (HAART), exposure to measles virus, and revaccination among children infected

27 surveillance confirmed that transmission of measles virus, and therefore measles deaths, had been re

28 implications for pathogens, such as HIV and measles virus, and tumors that evade the immune response

29 , respectively, had seroprotective levels of measles virus antibodies; 100.0% and 99.6%, respectively

30 The measles virus antibody avidity indexes were high for all

31 e MV schedule was associated with protective measles virus antibody levels at 24 months of age in nea

32 At 4.5 months of age, 75% had nonprotective measles virus antibody levels.

33 We tested the measles virus antibody response at 4.5, 9, 18, and 24 mo

34 The measles virus antibody titer, however, is a potency requ

35 since 1963 resulted in a decrease in average measles virus antibody titers among plasma donors, which

36 To mitigate the decline in measles virus antibody titers in IVIGs and to ensure con

37 Neutralizing measles virus antibody titers were above the threshold f

38 Antiviral agents against measles virus are not commercially available but could b

39 unosuppression as well as the application of measles virus as an oncolytic therapeutic.

40 efense against various RNA viruses including measles virus; as such, many viruses have evolved strate

41 ph node and spleen cells with UV-inactivated measles virus at various time points after infection, ga

42 e predicted potential interface areas of the measles virus attachment protein hemagglutinin to begin

43 either one of three escalating doses of the measles-virus-based candidate vaccine (low dose [1.5 x 1

44 This vaccine is the first promising measles-virus-based candidate vaccine for use in human b

45 dose (n=12), or the high dose (n=12) of the measles-virus-based candidate vaccine, or Priorix (n=6),

46 The live recombinant measles-virus-based chikungunya vaccine had good immunog

47 unogenicity and safety of a live recombinant measles-virus-based chikungunya vaccine.

48 ination and were likely exposed to wild-type measles virus, but none were reported to have had clinic

49 Europe, and the USA show the ease with which measles virus can re-enter communities if high levels of

50 he characterization of mechanisms underlying measles virus clinical disease has been hampered by the

51 We also found that measles virus colocalized to lipid rafts in both acute a

52 h antibodies to HIV-1 also had antibodies to measles virus, compared with 568 (71%) of 796 children w

53 Rhinovirus and measles viruses each require ASMase activity during earl

54 The new targeted virus was named measles virus echistatin vector (MV-ERV).

55 hat hsp70-dependent stimulation of Edmonston measles virus (Ed MeV) transcription caused an increased

56 The oncolytic measles virus Edmonston strain (MV-Edm), a nonpathogenic

57 The measles virus entry concert has four movements.

58 While measles virus entry depends on a receptor-binding protei

59 to the membrane interaction data of HRC4, a measles virus entry inhibitor peptide, revealing its inc

60 ddress whether preassembly reflects a unique measles virus entry strategy, we characterized the prote

61 Here, we show that measles virus escapes MDA5 detection by targeting the ph

62 h significantly impacts our understanding of measles virus evolution.

63 A recombinant measles virus expressing a mutant V protein deficient in

64 Our results show that Ad35 competes with measles virus for binding to CD46 but not with complemen

65 sease virus, a paramyxovirus and relative of measles virus, forms dimers that assemble into pseudotet

66 ional 186 cases (7%) resulted from spread of measles virus from these imported cases, and 388 cases (

67 Our results demonstrate that measles virus functionally varies conserved elements of

68 Chimeric peptides incorporating the measles virus fusion "promiscuous" T cell epitope via a

69 iochemical conditions at the cell surface on measles virus fusion complexes.

70 demonstrate aptazyme-dependent regulation of measles virus fusion protein expression, translating int

71 protein-deficient (C-protein-knockout [CKO]) measles viruses generated about 10 times more DI-RNAs th

72 project to date, revealing novel aspects of measles virus genetics and providing new insights into t

73 es, and 28 cases associated with an imported measles virus genotype.

74 Eighth, tracking measles virus genotypes is critical to determining if an

75 Measles virus genotypes were determined by reverse-trans

76 ons that could be homologous to those in the measles virus H attachment glycoprotein known to be invo

77 The Edmonston vaccine strain of measles virus has potent and selective activity against

78 sly shown that attenuated vaccine strains of measles virus have potent antitumor activity against gli

79 lobular heads to the tetrameric stalk of the measles virus hemagglutinin (H), we asked whether and ho

80 The measles virus hemagglutinin (MeV-H) protein is the main

81 two Sindbis virus DNA vaccines encoding the measles virus hemagglutinin (pMSIN-H) and fusion protein

82 which areas of Bacillus anthracis toxins and measles virus hemagglutinin protein interact with their

83 loops, the association of nectin-4 with the measles virus hemagglutinin requires only the BC and FG

84 solved structure of the globular head of the measles virus hemagglutinin suggests that this differenc

85 ine measles virus (vac2) and for a wild-type measles virus (IC323) as early as passage 1 after virus

86 learly define the molecular determinants for measles virus IFN evasion and validate specific targets

87 We previously demonstrated in measles virus-infected cells that PKR is required for th

88 antiapoptotic host factor in the context of measles virus infection and suggest that the antiapoptot

89 Our findings suggest that measles virus infection during pregnancy confers a high

90 Serological evidence of measles virus infection has been detected among people e

91 The most severe sequela of measles virus infection is subacute sclerosing panenceph

92 Our data indicate that measles virus infection leads to a decrease in IL-12 sec

93 Measles virus infection leads to immune suppression.

94 Chronic measles virus infection of the brain causes subacute scl

95 male who developed focal, chronic persistent measles virus infection of the brain following interfero

96 us, although the precise role of ADAR during measles virus infection remains unknown.

97 y the events underlying acute and persistent measles virus infection, we performed a global transcrip

98 as an enhancer of IFN-beta induction during measles virus infection.

99 e of virus infection from lung tissue during measles virus infection.

100 und no evidence that persons with inapparent measles virus infections shed measles virus.

101 ls infected with vesicular stomatitis virus, measles virus, influenza A virus, and Nyamanini virus, w

102 virus, Venezuelan equine encephalitis virus, measles virus, influenza A virus, reovirus, vesicular st

103 ve investigated the steps governing entry of measles virus into SLAMF1-positive cells and identified

104 Measles virus is a highly contagious virus that, despite

105 evolution of new MeV subgenotypes.IMPORTANCE Measles virus is a paradigmatic RNA virus, as the antige

106 The V protein of measles virus is an important virulence factor that can

107 Live attenuated measles virus is one of the most efficient and safest va

108 Measles virus is transmitted by the respiratory route an

109 The causative agent, measles virus, is a small enveloped RNA virus that infec

110 27 complete genomes from H1 and D8 genotype measles viruses isolated from outbreak cases, we estimat

111 virus, varicella-zoster virus, mumps virus, measles virus, lyssavirus, herpes simplex viruses 1 and

112 The pH-independent measles virus membrane fusion process begins when the at

113 -PCR (RT-PCR) method specific for genotype A measles virus (MeV) (MeVA RT-quantitative PCR [RT-qPCR])

114 The measles virus (MeV) attachment (H) protein stalk domain

115 uitous pathogens of humans and animals, with measles virus (MeV) being a prominent one.

116 sp70) is host protective in a mouse model of measles virus (MeV) brain infection.

117 Using measles virus (MeV) fusion complexes, we demonstrate tha

118 ldwide that have caused localized outbreaks, measles virus (MeV) has regained importance as a pathoge

119 on after infection of susceptible cells with measles virus (MeV) have often reported greater IFN synt

120 Although such cases are infrequent, measles virus (MeV) infection can occur in vaccinated in

121 nhuman primates are naturally susceptible to measles virus (MeV) infection.

122 Clearance of measles virus (MeV) involves rapid elimination of infect

123 Measles virus (MeV) is known to be highly contagious, wi

124 Measles virus (MeV) is the poster child for acute infect

125 The measles virus (MeV) membrane fusion apparatus consists o

126 Measles virus (MeV) N features an amino-terminal RNA-bin

127 Measles virus (MeV) neutralizing antibody concentrations

128 n both intact and trypsin-cleaved sedimented measles virus (MeV) nucleocapsids under ultra-fast magic

129 of loosely assembled tetramers from purified measles virus (MeV) particles and cells transiently expr

130 The measles virus (MeV) phosphoprotein (P) tethers the polym

131 argets of infection, and these cells traffic measles virus (MeV) to lymph nodes for amplification and

132 nd whether SVF cases contribute to continued measles virus (MeV) transmission.

133 The negative-strand RNA virus measles virus (MeV) uses tissue-specific nectin-4, and t

134 The measles virus (MeV), a member of the paramyxovirus famil

135 Measles virus (MeV), a morbillivirus within the paramyxo

136 ganization of functional fusion complexes of measles virus (MeV), an archetype of the paramyxovirus f

137 (NiV), human parainfluenza virus 3 (HPIV3), measles virus (MeV), mumps virus (MuV), and respiratory

138 iverse Paramyxovirus L proteins derived from measles virus (MeV), Nipah virus (NiV), and respiratory

139 MVDP induced robust measles virus (MeV)-specific humoral and T-cell response

140 e fusion and syncytium formation mediated by measles virus (MeV).

141 hemagglutinin (H) and fusion (F) proteins of measles virus (MeV).

142 th a microbial sensor and entry receptor for measles virus (MeV).

143 t is increasingly difficult to differentiate measles viruses (MeVs) relating to certain outbreaks on

144 za virus type 2, parainfluenza virus type 5, measles virus, mumps virus, Hendra virus, and Nipah viru

145 Paramyxovirus pathogens include measles virus, mumps virus, human respiratory syncytial

146 ail of the F proteins of the paramyxoviruses measles virus, mumps virus, Newcastle disease virus, hum

147 ortions of the samples were seropositive for measles virus, mumps virus, or rubella virus antibodies,

148 many medically important viruses, including measles virus, mumps virus, parainfluenza viruses, respi

149 en extended to predict genes for 12 viruses: measles virus, mumps virus, rubella virus, respiratory s

150 The measles virus (MV) accessory proteins V and C play impor

151 versely, PKR amplifies IFN-beta induction by measles virus (MV) and inhibits virus protein synthesis.

152 Measles virus (MV) and lymphocytic choriomeningitis viru

153 The V proteins of measles virus (MV) and parainfluenza virus 5 (PIV5) were

154 Dendritic cells (DCs) are targets of measles virus (MV) and play central roles in viral disse

155 Clinical trials of oncolytic attenuated measles virus (MV) are ongoing, but successful systemic

156 bility to form functional complexes with the measles virus (MV) attachment protein (H).

157 mma interferon (IFN-gamma) for survival of a measles virus (MV) challenge; however, the direct role o

158 nfirmed in our Treg-sensitive mouse model of measles virus (MV) CNS infection, in which we observed m

159 Measles virus (MV) constitutes a principal cause of worl

160 After the contagion measles virus (MV) crosses the respiratory epithelium wi

161 e the mechanism(s) by which coinfection with measles virus (MV) decreases HIV-1 replication, we estab

162 72-responsive virus using the mouse model of measles virus (MV) encephalitis.

163 Measles virus (MV) entry requires at least 2 viral prote

164 etion of its G glycoprotein and encoding the measles virus (MV) fusion (F) and hemagglutinin (H) enve

165 In particular, the measles virus (MV) fusion (F) protein executes membrane

166 The measles virus (MV) fusion (F) protein trimer executes me

167 The measles virus (MV) fusion apparatus consists of a fusion

168 e scheme potential, we engineered infectious measles virus (MV) genomic cDNAs with a vaccine strain b

169 tion method for identification of most known measles virus (MV) genotypes was developed.

170 However, acute infection with measles virus (MV) has been found to suppress HIV-1 repl

171 Edmonston vaccine strains of measles virus (MV) have shown significant antitumor acti

172 Edmonston vaccine strains of measles virus (MV) have significant antitumor activity i

173 Based on the identification of measles virus (MV) hemagglutinin (H) amino acids support

174 s (NDV) hemagglutinin-neuraminidase (HN) and measles virus (MV) hemagglutinin (H) proteins reside ent

175 s virus replicon-based DNA vaccines encoding measles virus (MV) hemagglutinin (H, pMSIN-H) or both he

176 Measles virus (MV) hemagglutinin (MV-H) and fusion (MV-F

177 is virus replicon particles that express the measles virus (MV) hemagglutinin (SIN-H) or fusion (SIN-

178 Measles virus (MV) immunosuppression is due to infection

179 between the remarkable genetic stability of measles virus (MV) in the field and the high mutation ra

180 Oncolytic measles virus (MV) induces cell fusion and cytotoxicity

181 amined expression of the chemokine RANTES in measles virus (MV) infected hippocampal neurons and quan

182 Measles virus (MV) infection causes an acute illness tha

183 Measles virus (MV) infection causes an acute illness tha

184 Measles virus (MV) infection is the major cause of vacci

185 Measles virus (MV) infection is undergoing resurgence an

186 Measles virus (MV) infection is undergoing resurgence an

187 In contrast, measles virus (MV) infection leads to downregulation of

188 ies of primate models suggest that wild-type measles virus (MV) infects immune cells located in the a

189 gG) antibodies can also enhance the entry of measles virus (MV) into monocytes and macrophages.

190 Measles virus (MV) is an important human pathogen that i

191 Measles virus (MV) is one of the most infectious pathoge

192 Measles virus (MV) is one of the most infectious pathoge

193 Measles virus (MV) lacking expression of C protein (C(KO

194 The hemagglutinin (H) protein of measles virus (MV) mediates attachment to cellular recep

195 SSPE brain plasma cell clones recognized the measles virus (MV) nucleocapsid protein, confirming that

196 ype [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficien

197 Imported measles virus (MV) outbreaks are maintained by poor vacc

198 The measles virus (MV) P gene codes for three proteins: P, a

199 The measles virus (MV) P gene encodes three proteins (P, V,

200 The current model of measles virus (MV) pathogenesis implies that apical infe

201 which measures immunoglobulin G (IgG) to all measles virus (MV) proteins, and the plaque reduction ne

202 the clinical manifestations and kinetics of measles virus (MV) replication in MV-vaccinated and unva

203 mouse central nervous system (CNS) neurons, measles virus (MV) spreads in the absence of hallmark vi

204 We generated measles virus (MV) strains defective for the expression

205 Wild-type measles virus (MV) strains use the signaling lymphocytic

206 We show here for measles virus (MV) that particle activation can be made

207 70-kDa heat shock protein (hsp72) increases measles virus (MV) transcription and genome replication.

208 The discovery that measles virus (MV) uses the adherens junction protein ne

209 re we report that in the cotton rat model of measles virus (MV) vaccination passively transferred MV-

210 licensure and generalization of an effective measles virus (MV) vaccine 41 years ago, antibody levels

211 The mechanisms of measles virus (MV) vaccine attenuation are insufficientl

212 Measles virus (MV) vaccine effectively protects seronega

213 Although live-attenuated measles virus (MV) vaccines have been used successfully

214 pounds specifically preventing fusion of the measles virus (MV) with target cells at IC(50) values of

215 Measles virus (MV), a member of the family Paramyxovirid

216 ction of the central nervous system (CNS) by measles virus (MV), biased hypermutations of the viral g

217 virus (VSV-FH), which is superior to that of measles virus (MV), in different cancer cell lines.

218 that specifically prevent fusion induced by measles virus (MV), most likely by interfering with conf

219 Measles virus (MV), one of the most contagious viruses i

220 other paramyxoviruses, Sendai virus (SV) and measles virus (MV), or the TM domain of the unrelated gl

221 Measles virus (MV), while targeted for eradication, stil

222 CD20 antibody, we generated a CD20-targeted measles virus (MV)-based vector.

223 F4 and measles virus (MV)-specific cytokine producing T cell re

224 To characterize the measles virus (MV)-specific T cell responses important f

225 hemagglutinin (H) and fusion (F) proteins of measles virus (MV).

226 SLAM; CD150) is the immune cell receptor for measles virus (MV).

227 iple neurotropic viral infections, including measles virus (MV); however, the downstream pathways thr

228 Live attenuated Edmonston B strain of measles virus (MV-Edm) is a potent and specific oncolyti

229 lower than the parental Edmonston strain of measles virus (MV-Edm), but it selectively infected Chin

230 nodeficient mice following oncolytic vaccine measles virus (MV-Vac) treatment.

231 We previously showed that vectored measles viruses (MV) expressing HBsAg retain measles vac

232 Here, we describe oncolytic measles viruses (MV) retargeted to CD133.

233 Recombinant measles viruses (MVs) are in clinical trials as cancer t

234 n HCV vaccine, we engineered two recombinant measles viruses (MVs) expressing structural proteins fro

235 we tested the effect of ADAR1 deficiency on measles virus (MVvac strain) growth and virus-induced ce

236 virus P NBD binds to residues 477 to 505 of measles virus N with 1:1 stoichiometry.

237 For measles virus N, the binding site for the P protein maps

238 inding sites of several pathogens, including measles virus, Neisseria gonorrhea, and human herpesviru

239 d-type infection stimulates higher levels of measles-virus-neutralizing antibodies (mnAbs) than does

240 nally imported case (42%) or had a strain of measles virus not endemic in the United States (12%).

241 from 3 patients with PD and determined that measles virus nucleocapsid protein (MVNP) was expressed

242 nsically disordered C-terminal domain of the measles virus nucleoprotein (N(TAIL)) were cyanylated at

243 K18 domain from Tau protein and N(TAIL) from measles virus nucleoprotein.

244 sing either live viruses (dengue, mumps, and measles viruses) or nucleic acid material (Nipah and chi

245 These include GB virus C, measles virus, Orientia tsutsugamushi, and human T lymph

246 e in the age-specific force of infection for measles virus over time.

247 Measles virus P and N interact through two binding sites

248 The measles virus P gene products V and C antagonize the hos

249 However, only in measles virus P is the NBD stable and folded, having a l

250 tration calorimetry, we demonstrate that the measles virus P NBD binds to residues 477 to 505 of meas

251 ids of both measles virus and mumps virus P (measles virus P, 457 to 507; mumps virus P, 343 to 391)

252 had higher lymphoproliferative responses to measles virus (P=.01) and mumps virus (P=.006).

253 sociated with high levels of IgG antibody to measles virus (P=.09) but low levels of IgG antibody to

254 Few public health laboratories sequence measles virus-positive specimens to determine genotype,

255 rsus MMR-unrelated febrile seizures) and the measles virus receptor CD46 (rs1318653: P = 9.6 x 10(-11

256 ons, which ablate recognition of the natural measles virus receptors CD46 and SLAM.

257 Measles virus remains a significant cause of mortality i

258 Measles virus remains a substantial cause of morbidity a

259 Using a whole cell measles virus replication assay, we describe here some a

260 mmunodeficiency virus-1, Ebola, Marburg, and measles virus replication, suggesting that it may be a n

261 rs was based on a phenotypic assay measuring measles virus replication.

262 osis of SSPE were tested for the presence of measles virus RNA.

263 Our results indicate that CD133-targeted measles viruses selectively eliminate CD133(+) cells fro

264 The measles virus sequences derived from brain tissue sample

265 Enzyme immunoassay was used to analyze measles virus-specific IgG levels, avidity maturation, a

266 Collection of measles virus specimens from cases for genetic analysis

267 Measles virus spreads rapidly and efficiently in human a

268 In summary, EGFRvIII-retargeted oncolytic measles virus strains have comparable therapeutic effica

269 This report describes measles virus surveillance in the United States for 1989

270 erestingly, l-ddBCNAs also inhibit wild type measles virus syncytia formation with a TCID(50) of 7.5

271 e synthesized alone and also linked with the measles virus T cell epitope to produce a chimeric pepti

272 tor based on the Edmonston vaccine strain of measles virus targeted to integrin alpha(v)beta3, which

273 hough similar numbers of influenza virus and measles virus tetramer-positive cells were generated by

274 Using six retargeted measles viruses that bind to Her-2/neu with a 5-log rang

275 Five of eight recombinant IgGs recognized measles virus, the cause of subacute sclerosing panencep

276 s learned from the successful end of endemic measles virus transmission (i.e., elimination) in the Un

277 he Americas successfully interrupted endemic measles virus transmission 8 years after setting a regio

278 Americas set a goal of interrupting endemic measles virus transmission by the end of 2000.

279 emain an important strategy for interrupting measles virus transmission in the European Region, altho

280 Endemic measles virus transmission was interrupted in 2002.

281 llance system is geared towards detection of measles virus transmission, rapid discovery of measles o

282 ity to measles was insufficient to interrupt measles virus transmission.

283 formation was used to generate a recombinant measles virus unable to antagonize STAT1 function (STAT1

284 Expression of measles virus V cDNA can delay cell death induced by gen

285 scriptional assays reveal that expression of measles virus V cDNA inhibits p73, but not p53.

286 thic effects than the wild type, implicating measles virus V protein as an inhibitor of cell death.

287 ins that copurify with ectopically expressed measles virus V protein has revealed interactions with D

288 y conserved C-terminal zinc finger domain of measles virus V protein is both necessary and sufficient

289 A more direct target for measles virus V protein-mediated IFN-alpha/beta evasion

290 independent rescue events both for a vaccine measles virus (vac2) and for a wild-type measles virus (

291 protected only in conjunction with the live measles virus vaccine boost.

292 n administered alone or followed by the live measles virus vaccine in cotton rats.

293 ication of the enveloped Ebola, Marburg, and measles viruses was inhibited with Rab9 siRNA, although

294 ynthetic or natural dsRNAs or infection with measles virus, we observed increased mRNA but decreased

295 Measles virus, while being targeted for eradication, sti

296 escribe the rescue and characterization of a measles virus with a specific mutation in the stalk regi

297 Recombinant measles virus with an engineered deficiency in V protein

298 The interaction of measles virus with its receptor signaling lymphocytic ac

299 athogenic myxoviruses (influenza A virus and measles virus) with comparable replication kinetics, we

300 erological evidence of exposure to wild-type measles virus without a reported history of measles.