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

6 the avidity of antibodies were measured for measles virus.

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

8 rization of currently circulating strains of measles viruses.

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

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

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

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

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

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

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

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

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

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

19 modeling to determine the divergence date of measles virus and rinderpest virus.

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

21 We sequenced the genome of a 1912 measles virus and used selection-aware molecular clock m

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

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

29 The measles virus antibody avidity indexes were high for all

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

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

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

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

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

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

36 Neutralizing measles virus antibody titers were above the threshold f

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

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

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

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

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

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

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

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

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

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

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

48 operty for infection of the brain.IMPORTANCE Measles virus can invade the central nervous system (CNS

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

50 omplex, central nervous system (CNS)-adapted measles virus can spread outside the CNS within an infec

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

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

53 ntibodies to respiratory syncytial virus and measles virus, compared to uninfected controls.

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

55 Levels of antibodies induced by the measles virus-containing vaccine have been shown to decl

56 Rhinovirus and measles viruses each require ASMase activity during earl

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

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

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

60 The measles virus entry concert has four movements.

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

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

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

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

65 h significantly impacts our understanding of measles virus evolution.

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

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

68 TA cards for the detection and genotyping of measles virus from clinical samples has not been evaluat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 ly enrolled for serological testing for anti-measles virus immunoglobulin G antibody.

87 virus, vesicular stomatitis virus (VSV), and measles virus in GBA knockout cells.

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

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

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

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

92 Measles virus infection leads to immune suppression.

93 Chronic measles virus infection of the brain causes subacute scl

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

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

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

97 d children before and 2 months after natural measles virus infection.

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 Measles virus infects immune cells, causing acute immune

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 ped viruses tested, including herpesviruses, Measles virus, influenza, and SARS-CoV-2.

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

105 pidemiology of international importations of measles virus into the United States during the postelim

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

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

108 Measles virus is directly responsible for more than 100,

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

110 Measles virus is transmitted by the respiratory route an

111 The genetic characterization of measles viruses is an important tool for measles surveil

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

113 27 complete genomes from H1 and D8 genotype measles viruses isolated from outbreak cases, we estimat

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

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

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

117 human parainfluenza virus type-3 (HPIV3) and measles virus (MeV) are a substantial health threat.

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

119 A clinical isolate of measles virus (MeV) bearing a single amino acid alterati

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

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

122 We show that the measles virus (MeV) C protein is an additional component

123 During a measles virus (MeV) epidemic in 2009 in South Africa, me

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

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

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

127 these animal models) than wt MeV.IMPORTANCE Measles virus (MeV) infection can be severe in immunocom

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

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

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

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

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

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

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

135 Measles virus (MeV) neutralizing antibody concentrations

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

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

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

139 ons of chemokine CXCL10 in 288 patients with measles virus (MeV) primary infection and 16 patients wi

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

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

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

143 ented negative-strand RNA viruses, including measles virus (MeV), a member of the Paramyxoviridae fam

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

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

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

147 antibody titers to hepatitis A virus (HAV), measles virus (MeV), and cytomegalovirus (CMV).

148 Measles virus (MeV), like all viruses of the order Monon

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

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

151 Here, we generated measles virus (MeV)-based vaccine candidates expressing

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

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

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

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

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

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

158 ARS/MERS), human enteroviruses/rhinoviruses, measles virus, mumps virus, Hepatitis A-E Virus, Chikung

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 72-responsive virus using the mouse model of measles virus (MV) encephalitis.

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

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

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

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

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

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

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

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

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

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

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

185 Measles virus (MV) immunosuppression is due to infection

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

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

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

189 Measles virus (MV) infection is undergoing resurgence an

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

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

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

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

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

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

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

197 Using a mouse model of measles virus (MV) neuronal infection, we show that MV R

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

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

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

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

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

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

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

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

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

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

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

209 70-kDa heat shock protein (hsp72) increases measles virus (MV) transcription and genome replication.

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

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

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

213 Measles virus (MV) vaccine effectively protects seronega

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

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

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

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

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

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

231 ial from many neurotropic RNA viruses (e.g., measles virus [MV], West Nile virus [WNV], Sindbis virus

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

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

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

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

236 Measles virus neutralizing antibodies were also measured

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

238 Preventing measles virus nosocomial transmission likely decreases m

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

240 ed a recently developed approach to assemble measles virus nucleocapsid-like particles on specific se

241 nsically disordered C-terminal domain of the measles virus nucleoprotein (N(TAIL)) and the X domain (

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

246 Measles virus P and N interact through two binding sites

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

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

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

250 otein (N(TAIL)) and the X domain (XD) of the measles virus phosphoprotein complex.

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

252 Our analyses show that the measles virus potentially arose as early as the sixth ce

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

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

255 ation factories in infected cells.IMPORTANCE Measles virus remains a pathogen of significant global c

256 Measles virus remains a significant cause of mortality i

257 Measles virus remains a substantial cause of morbidity a

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

259 Measles virus replication occurs in the cytoplasm in ass

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

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

262 Seven studies reporting on measles virus-specific cellular immune responses found t

263 Measurement of measles virus-specific IgG is used to assess presumptive

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

265 decrease in the concentration and avidity of measles virus-specific neutralizing antibodies, compared

266 Measles virus-specific neutralizing antibody concentrati

267 Measles virus spreads rapidly and efficiently in human a

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

269 nfluenza virus, modest for VSV, and mild for measles virus, suggesting a greater role for viruses tha

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

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

274 nisms used by morbilliviruses, including the measles virus, to promote massive amplification within t

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

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

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

278 Endemic measles virus transmission was interrupted in 2002.

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

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

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

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

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

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

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

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

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

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

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

290 susceptible to viruses, including the YF and measles virus vaccine strains, in the absence or presenc

291 macaques were immunized and boosted with the measles virus-vectored chikungunya vaccine or sham-vacci

292 A new measles virus-vectored vaccine was developed to prevent

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.