ライフサイエンスコーパス: HPIV3

1 ne against human parainfluenza virus type 3 (HPIV3).

2 (NDV), and human parainfluenza virus type 3 (HPIV3).

3 l vaccine for protection against human PIV3 (hPIV3).

4 protein of human parainfluenza virus type 3 (HPIV3).

5 ed by antibodies to EV than by antibodies to HPIV3.

6 enes in the promoter proximal position of rB/HPIV3.

7 ced a robust immune response to both RSV and HPIV3.

8 re lower respiratory tract disease caused by HPIV3.

9 ndidate to protect against illness caused by HPIV3.

10 were protected from challenge with wild-type HPIV3.

11 e a bivalent mucosal vaccine against RSV and HPIV3.

12 tablish an effective antiviral state against HPIV3.

13 provides a bivalent vaccine against RSV and HPIV3.

14 ble from that conferred by immunization with HPIV3.

15 e genes of bPIV3 were replaced with those of hPIV3.

16 induced by previous infection with wild-type HPIV3.

17 cted hamsters completely upon challenge with hPIV3.

18 o confer bivalent protection against RSV and HPIV3.

19 play an important role in the replication of HPIV3.

20 rected against both surface glycoproteins of hPIV3.

21 didates for dual protection against HMPV and HPIV3.

22 nal titers were comparable to wild-type (wt) HPIV3.

23 l genomes and all 13 samples had >1 read for HPIV3.

24 was increased for the mutants compared to wt HPIV3.

25 opment as a bivalent vaccine against RSV and HPIV3.

26 izing antibodies in hamsters against RSV and HPIV3.

27 haps other paramyxoviruses, such as hRSV and hPIV3.

28 level of resistance to challenge with RSV or HPIV3 28 days later.

29 ive by RT-PCR, including 66 HRSV, 2 HPIV2, 5 HPIV3, 3 influenza A virus, and 10 influenza B virus spe

30 n a high-throughput screen for inhibitors of HPIV3 (a major cause of acute respiratory infection), we

31 yxoviruses-human parainfluenza virus type 3 (HPIV3), a major cause of lower respiratory tract disease

32 Human parainfluenza virus type 3 (HPIV3), a paramyxovirus, is a major viral cause of sever

33 bovine/human parainfluenza virus type 3 (rB/HPIV3), a recombinant bovine PIV3 (rBPIV3) in which the

34 attenuated recombinant bovine/human PIV3 (rB/HPIV3), a recombinant BPIV3 in which the bovine HN and F

35 of nonhuman primates compared to human PIV3 (HPIV3), an important pathogen of infants and young child

36 phosphorylated forms of GAPDH associate with HPIV3 and are involved in the regulation of virus gene e

37 IV3-F(H)HN(H) as a vaccine candidate against HPIV3 and as a vector for other viral antigens is discus

38 glycoprotein substitution on replication of HPIV3 and BPIV3 in the upper and lower respiratory tract

39 grew to titers comparable to those of their HPIV3 and BPIV3 parents in LLC-MK2 monkey kidney and Mad

40 keys to a level intermediate between that of HPIV3 and BPIV3.

41 ng monoclonal antibodies, one targeting both HPIV3 and HPIV1 and the other targeting both RSV and HMP

42 Both HPIV3 and NDV HNs are sensitive to receptor-binding inhi

43 ee-dimensional structural information on the HPIV3 and NDV HNs, we propose mechanisms for the observe

44 asal route, a route that has been shown with HPIV3 and respiratory syncytial virus vaccines to be rel

45 terminal heptad repeat (HRN) domains of both HPIV3 and RSV F with high affinity.

46 V3 F that potently inhibit infection by both HPIV3 and RSV.

47 is a candidate bivalent live vaccine against HPIV3 and RSV.

48 o protect infants and young children against HPIV3 and SARS-CoV-2.

49 iently in cells simultaneously infected with HPIV3 and treated with IFN-gamma, indicating that the in

50 Infection of HAE cells with wild-type HPIV3 and variant viruses closely reflects that seen in

51 es such as human parainfluenza virus type-3 (HPIV3) and measles virus (MeV) are a substantial health

52 including respiroviruses (that is, HPIV1 and HPIV3) and morbilliviruses (that is, MeV).

53 ng RNAs of human parainfluenza virus type 3 (HPIV3) and packaging of these proteins within purified v

54 Human parainfluenza virus 3 (HPIV3) and respiratory syncytial virus (RSV) cause lower

55 ne against human parainfluenza virus type 3 (HPIV3) and respiratory syncytial virus (RSV) subgroups A

56 virus 5 (PIV5), human parainfluenza virus 3 (HPIV3), and respiratory syncytial virus (RSV) infections

57 ompared to human parainfluenza virus type 3 (HPIV3), and the Ka strain also was shown to be attenuate

58 was similar to that of their parent virus rB/HPIV3, and each of the chimeras induced a robust immune

59 a virus as well as the paramyxoviruses PIV5, HPIV3, and RSV.

60 A synthetase had no antiviral effect against HPIV3; and (iii) primary transcription occurred in the a

61 on resulted in only modest decreases in anti-HPIV3 antibodies in sera and was sufficient to confer co

62 nation inhibition assay was used to quantify hPIV3 antibody.

63 Varying the HPIV3 antigen insertion site and vector dose allowed fin

64 cis-element involved in the synthesis of the HPIV3 antigenomic RNA.

65 Currently, vaccines against hPIV3 are in clinical trials but none have been approved

66 atric clinical evaluation.IMPORTANCE RSV and HPIV3 are the first and second leading viral causes of s

67 irus (HMPV) and human parainfluenza virus 3 (HPIV3) are among the leading causes of severe pediatric

68 irus (HMPV) and human parainfluenza virus 3 (HPIV3) are important pediatric pathogens and need effect

69 (RSV) and human parainfluenza virus type 3 (HPIV3) are major pediatric respiratory pathogens that la

70 (RSV) and human parainfluenza virus type 3 (HPIV3) are major viral agents of acute pediatric bronchi

71 hMPV), and human parainfluenza virus type 3 (hPIV3) are responsible for the majority of pediatric res

72 (RSV) and human parainfluenza virus type 3 (HPIV3) are the first and second leading viral agents of

73 (RSV) and human parainfluenza virus type 3 (HPIV3) are two major causes of pediatric pneumonia and b

74 pathogen, human parainfluenza virus type 3 (HPIV3), as a vaccine vector against Ebola virus.

75 STAT1 activation was not affected by HPIV3 at early postinfection times but was partially inh

76 An attenuated chimeric bovine/HPIV3 (B/HPIV3) based on bovine PIV3, with fusion (F) an

77 An attenuated chimeric bovine/HPIV3 (B/HPIV3) based on bovine PIV3, with fusion (F) and hemaggl

78 HPIV3 bearing the BPIV3 F and HN genes was restricted in

79 hPIV1 and hPIV3 bind modifications of Neu5Acalpha2-3Galbeta1-4GlcN

80 cation was similar to that of wild-type (wt) HPIV3 both in vitro and in vivo.

81 ined regions of HPIV3 F inhibit infection by HPIV3 by interfering with the structural transitions of

82 correlated with the greater potential of the HPIV3 C peptide to interact with the HeV F N peptide coi

83 n paramyxoviruses, including hRSV, hMPV, and hPIV3, cause the majority of acute upper and lower respi

84 ing antibodies and conferred protection from HPIV3 challenge in cotton rats.

85 ric viruses induced a level of resistance to HPIV3 challenge in these animals which was indistinguish

86 wt and provided complete protection against HPIV3 challenge.

87 tested resulted in complete protection from HPIV3 challenge.

88 ufficient to confer complete protection from HPIV3 challenge.

89 tenuation, and immunogenicity of these BPIV3/HPIV3 chimeras suggest that the modified Jennerian appro

90 llular proteins potentially interacting with HPIV3 cis-acting regulatory RNAs, a gel mobility shift a

91 ely little is known about the Ab response to HPIV3 compared with other pathogens, such as influenza v

92 ecombinant human parainfluenza type 3 virus (HPIV3) containing BPIV3 F and HN glycoprotein genes in p

93 romoter of human parainfluenza virus type 3 (HPIV3) contains multiple cis-elements controlling transc

94 F protective antigens are replaced by their HPIV3 counterparts (48).

95 the F and HN genes were replaced with their HPIV3 counterparts, was used to express the major protec

96 common attenuated backbone, specifically rB/HPIV3 derivatives expressing the G and/or F major protec

97 Because immunization for the prevention of HPIV3 disease must occur in early infancy when maternal

98 Sendai virus mouse surrogate model of human HPIV3 disease when administered therapeutically 48 h aft

99 Moreover, 1 aerosol HPIV3/EboGP dose conferred 100% protection to macaques e

100 gle intranasal inoculation of 10(5.3) PFU of HPIV3/EboGP or HPIV3/EboGP-NP showed no apparent signs o

101 Serum and mucosal samples from aerosolized HPIV3/EboGP recipients exhibited high EBOV-specific IgG,

102 The HPIV3/EboGP vaccine induced an EBOV-specific cellular re

103 The HPIV3/EboGP vaccine produced a more robust cell-mediated

104 HPIV3/EboGP was 100-fold more efficiently neutralized by

105 hat expresses the glycoprotein (GP) of EBOV (HPIV3/EboGP) delivered to the respiratory tract.

106 e EV structural glycoprotein (GP) by itself (HPIV3/EboGP) or together with the EV nucleoprotein (NP)

107 us macaques were vaccinated with aerosolized HPIV3/EboGP, liquid HPIV3/EboGP, or an unrelated, intram

108 cinated with aerosolized HPIV3/EboGP, liquid HPIV3/EboGP, or an unrelated, intramuscular, Venezuelan

109 inoculation of 10(5.3) PFU of HPIV3/EboGP or HPIV3/EboGP-NP showed no apparent signs of disease yet d

110 or together with the EV nucleoprotein (NP) (HPIV3/EboGP-NP).

111 In B/HPIV3 empty vector-immunized hamsters, SARS-CoV-2 replic

112 B/HPIV3 expressing a codon-optimized pre-fusion stabilized

113 An attenuated HPIV3 expressing a major protective antigen of measles v

114 We recently showed that rB/HPIV3 expressing a partially stabilized prefusion form (

115 In hamsters, the rB/HPIV3 expressing wt G conferred better protection agains

116 rB/HPIV3 expressing wt RSV G provides a bivalent vaccine ag

117 recombinant consisting of BPIV3 bearing the HPIV3 F and HN genes (rBPIV3-F(H)HN(H)) were generated t

118 l neutralizing Abs against a small number of HPIV3 F epitopes have been identified to date, relativel

119 -neuraminidase (HN), suggesting that NDV and HPIV3 F have stricter requirements for homotypic HN for

120 Peptides derived from defined regions of HPIV3 F inhibit infection by HPIV3 by interfering with t

121 amyxovirus F or HN glycoproteins with either HPIV3 F or HN does not result in the formation of syncyt

122 HPIV3 F peptides were also effective in inhibiting HeV p

123 further studies were performed with a mutant HPIV3 F protein (F-KDEL) lacking a transmembrane anchor

124 the C-terminal heptad repeat (HRC) domain of HPIV3 F that potently inhibit infection by both HPIV3 an

125 A mutations cause SV5 WR F, but not NDV F or HPIV3 F, to be triggered to cause fusion in the absence

126 d to be down-regulated when coexpressed with HPIV3 F.

127 N(P-M) virus was attenuated compared to rSeV-HPIV3(F-HN) in LLC-MK2 cells, and yet both vaccine candi

128 accine candidates rSeV-HPIV3HN(P-M) and rSeV-HPIV3(F-HN) were constructed in which the HPIV3 HN open

129 reported that a human parainfluenza virus 3 (HPIV3) F peptide effectively inhibits infection mediated

130 ereas the virus expressing the RSV F ORF (rB/HPIV3-F1) was eightfold restricted compared to its rB/HP

131 mmunization of hamsters with rB/HPIV3-G1, rB/HPIV3-F1, or a combination of both viruses resulted in a

132 The human parainfluenza virus type 3 (HPIV3) fusion (F) and hemagglutinin-neuraminidase (HN) g

133 rus type 3 (PIV3) expressing the human PIV3 (hPIV3) fusion (F) and hemagglutinin-neuraminidase (HN) p

134 ecombinant PIV3 expressing the RSV G ORF (rB/HPIV3-G1) was not restricted in its replication in vitro

135 Immunization of hamsters with rB/HPIV3-G1, rB/HPIV3-F1, or a combination of both viruses

136 LA Protein participate in the regulation of HPIV3 gene expression.

137 Together, these data indicate that the HPIV3 gene product(s) is directly involved in the induct

138 ignals and inserted individually into the rB/HPIV3 genome in the promoter-proximal position preceding

139 trating that L dimerization is necessary for hPIV3 genome replication.

140 Human parainfluenza virus type 3 (HPIV3) genome RNA is transcribed and replicated by the v

141 lustering revealed the presence of identical HPIV3 genomic sequence in the two of the cases with hosp

142 We show that the molecular determinants for HPIV3 growth in vitro are fundamentally different from t

143 ne vector, human parainfluenza virus type 3 (HPIV3) has the advantages of needle-free administration

144 attenuated ones, developed higher levels of HPIV3 hemagglutination-inhibiting serum antibodies than

145 th measles virus (neutralizing antibody) and HPIV3 (hemagglutination inhibiting antibody) of over 1:5

146 coding the human parainfluenza virus type 3 (HPIV3) hemagglutinin-neuraminidase (HN) protein, a test

147 ion of the human parainfluenza virus type 3 (HPIV3) hemagglutinin-neuraminidase (HN), blocking recept

148 esponse most reliably by comparing bPIV3 and hPIV3 HI titers, and that bPIV3 vaccine prevents vaccine

149 However, in the upper respiratory tract, B/HPIV3/HMPV-F candidates were significantly more protecti

150 dy titers, similar to those induced by the B/HPIV3/HMPV-F candidates, and were similarly protected ag

151 nd could down-regulate surface expression of HPIV3 HN and heterologous HN/H proteins from simian viru

152 for a second receptor binding site near the HPIV3 HN dimer interface.

153 ggest that the two receptor binding sites on HPIV3 HN each contribute in distinct ways to virus-cell

154 This second binding site of HPIV3 HN is involved in triggering F.

155 eV-HPIV3(F-HN) were constructed in which the HPIV3 HN open reading frame and an additional gene junct

156 Newcastle disease virus (NDV) HN and HPIV3 HN respond differently to inhibition in ways that

157 d to result, in part, from an early block to HPIV3 HN synthesis, as well as an instability of the het

158 V HN-receptor binding is less sensitive than HPIV3 HN-receptor binding to 4-GU-DANA, while its neuram

159 a second receptor binding site (site II) on HPIV3 HN.

160 ynamics of human parainfluenza virus type 3 (HPIV3) HN/F pairs in living cells.

161 mples from 3 patients with hospital-acquired HPIV3 identified over a 12-day period on a general medic

162 d by the bPIV3 IgA and HI assays than by the hPIV3 IgA and HI assays, that bPIV3-induced antibody res

163 urthermore, MHC class II was also induced by HPIV3 in cells defective in class II transactivator, an

164 MHC class I was induced by HPIV3 in these cells at levels similar to those observed

165 MHC class II was also efficiently induced by HPIV3 in these cells.

166 RSV F open reading frame was evaluated in rB/HPIV3 in three forms: (i) pre-F without vector-packaging

167 B/HPIV3/S-2P replicated as efficiently as B/HPIV3 in vitro and stably expressed SARS-CoV-2 S.

168 toskeletal framework, in the reproduction of HPIV3 in vivo.

169 ription of human parainfluenza virus type 3 (HPIV3) in vitro.

170 HPIV3 induced both MHC class I and class II molecules in

171 (EMCV) and human parainfluenza virus type 3 (HPIV3), induced down-regulation of p53 in infected cells

172 antibody response can be differentiated from hPIV3-induced antibody response most reliably by compari

173 method to design vaccines to protect against HPIV3-induced disease in humans.

174 trate that human parainfluenza virus type 3 (HPIV3) induces incomplete autophagy by blocking autophag

175 The culture supernatant of HPIV3-infected cells also inhibited IFN-gamma-induced MH

176 ession was found to be strongly inhibited in HPIV3-infected cells.

177 Cumulative proportions of hPIV3 infection in young infants were further estimated

178 espiratory route to rhesus monkeys--in which HPIV3 infection is mild and asymptomatic--and were evalu

179 the basis of which cumulative proportions of hPIV3 infection were estimated to be 11% at 6 months of

180 the second dose exceeded that observed with HPIV3 infection, even though HPIV3 replicates much more

181 nti-HPIV3 titers similar to those induced by HPIV3 infection.

182 and epithelium-like (HT1080) cells following HPIV3 infection.

183 ess than that observed following a wild-type HPIV3 infection; however, the titer following the second

184 Human parainfluenza virus type 3 (HPIV3) infection causes severe damage to the lung epithe

185 of 12 cases of human parainfluenza virus 3 (HPIV3) infection that occurred among 64 allogeneic hemat

186 spital-acquired human parainfluenza 3 virus (HPIV3) infections at a children's hospital.

187 These data indicate that HPIV3 inhibits IFN-gamma-induced MHC class II expression

188 nd HPIV2 are best known to cause croup while HPIV3 is a common cause of bronchiolitis and pneumonia.

189 The attenuation of rB/HPIV3 is provided by the host range restriction of the B

190 Human parainfluenza virus type 3 (HPIV3) is a leading cause of illness in pediatric, older

191 Human parainfluenza virus type 3 (HPIV3) is a major pediatric respiratory pathogen lacking

192 Human parainfluenza virus type 3 (hPIV3) is a respiratory pathogen that can cause severe d

193 Human parainfluenza virus 3 (HPIV3) is a widespread pathogen causing severe and letha

194 Human parainfluenza virus type 3 (HPIV3) is one of the major causes of bronchiolitis, pneu

195 GHP-88309 showed nanomolar potency against HPIV3 isolates in well-differentiated human airway organ

196 Exposure histories and molecular analysis of HPIV3 isolates suggested that both community acquired an

197 ructure of human parainfluenza virus type 3 (hPIV3) L-P complex with the connector domain (CD') of a

198 The HPIV3 M-GE signal was previously shown to contain an app

199 On the basis of the assumption that hPIV3 maternal antibody decays exponentially and constan

200 timate the biologic half-life of human PIV3 (hPIV3) maternal antibody in young infants.

201 he gene-end (GE) transcription signal of the HPIV3 matrix (M) protein gene is identical to those of t

202 ah virus (NiV), human parainfluenza virus 3 (HPIV3), measles virus (MeV), mumps virus (MuV), and resp

203 neuraminidase activity impacts the extent of HPIV3-mediated fusion by releasing HN from contact with

204 Anti-IFN-beta, however, blocked the HPIV3-mediated induction of MHC class I only partially,

205 res luciferase reporter gene expression from HPIV3 minigenomes by viral proteins in a recombinant vac

206 ases 13 to 28 resulted in markedly decreased HPIV3 minireplicon replication, indicating these bases c

207 were critical in promoting replication of an HPIV3 minireplicon, while the intergenic sequence and N

208 orted that human parainfluenza virus type 3 (HPIV3) multiplication was inhibited by IFN-alpha in huma

209 ) from either BPIV3 Ka or SF in place of the HPIV3 N ORF.

210 lowering the pH (to approach the optimum for HPIV3 neuraminidase) decreased F triggering via release

211 le intranasal dose conferred serum HMPV- and HPIV3-neutralizing antibodies and provided protection in

212 vitro), all viruses induced titers of serum HPIV3-neutralizing antibodies similar to wt and provided

213 For human parainfluenza type 3 (HPIV3), one bifunctional site on HN can carry out both r

214 HPIV3 open reading frames (ORFs) encoding the nucleoprot

215 es of inhibitors bound to the HRN domains of HPIV3 or RSV F reveal remarkably different modes of bind

216 Infection by HPIV3 or RSV requires fusion of the viral and cell membr

217 of either human parainfluenza virus type 3 (HPIV3) or Nipah virus receptor binding proteins indicate

218 ein open reading frame (ORF) in place of the HPIV3 ORF, was modified to encode the measles virus hema

219 n additional, supernumerary gene between the HPIV3 P and M genes.

220 alyzed the human parainfluenza virus type 3 (HPIV3) P protein and deletion mutants thereof in an in v

221 was eightfold restricted compared to its rB/HPIV3 parent.

222 s resulted in RSV F being packaged in the rB/HPIV3 particle with an efficiency similar to that of RSV

223 y pathogen human parainfluenza virus type 3 (HPIV3), possess an envelope protein hemagglutinin-neuram

224 One bifunctional site (site I) on the HN of HPIV3 possesses both receptor binding and neuraminidase

225 ipients from developing antibody profiles of hPIV3 primary infection.

226 IV3 in primates, we produced viable chimeric HPIV3 recombinants containing the nucleoprotein (N) open

227 HPIV3 recombinants expressing the Ebola virus (Zaire spe

228 t observed with HPIV3 infection, even though HPIV3 replicates much more efficiently than NDV in these

229 parainfluenza virus types 1 and 3 (hPIV1 and hPIV3, respectively) to the glycan array of the Consorti

230 ivo and were found to be associated with the HPIV3 ribonucleoprotein complex in the infected cells.

231 The level of replication of rB/HPIV3-RSV chimeric viruses in the respiratory tract of r

232 V-neutralizing antibody titers induced by rB/HPIV3-RSV chimeric viruses were equivalent to those indu

233 version of the previously well-tolerated rB/HPIV3-RSV F vaccine candidate that induces a superior RS

234 Boosting instead with the rB/HPIV3-RSV-pre-F vectors resulted in efficient replicatio

235 s undetectable in nasal tissues and lungs; B/HPIV3/S and B/HPIV3/S-2P completely protected against we

236 B/HPIV3/S and B/HPIV3/S-2P replicated as efficiently as B/

237 ed significantly higher titers compared to B/HPIV3/S of serum SARS-CoV-2-neutralizing antibodies (12-

238 in nasal tissues and lungs; B/HPIV3/S and B/HPIV3/S-2P completely protected against weight loss afte

239 In hamsters, a single intranasal dose of B/HPIV3/S-2P induced significantly higher titers compared

240 B/HPIV3/S-2P is a promising vaccine candidate to protect i

241 B/HPIV3/S and B/HPIV3/S-2P replicated as efficiently as B/HPIV3 in vitro

242 In B/HPIV3/S-2P-immunized hamsters, infectious challenge viru

243 Furthermore, B/HPIV3/S-6P induced robust systemic and pulmonary S-speci

244 A single intranasal/intratracheal dose of B/HPIV3/S-6P induced strong S-specific airway mucosal immu

245 B/HPIV3/S-6P will be evaluated clinically as pediatric int

246 -2 prefusion-stabilized spike (S) protein (B/HPIV3/S-6P) and evaluated its immunogenicity and protect

247 In B/HPIV3/S-immunized hamsters, SARS-CoV-2 challenge virus w

248 his study, we aimed to characterize a set of HPIV3-specific Abs identified in multiple individuals fo

249 induced by infection with wild-type RSV, and HPIV3-specific antibody responses were similar to, or sl

250 nsisting of a chimeric bovine/human PIV3 (rB/HPIV3) strain expressing the RSV fusion (F) protein was

251 In this communication, we show that HPIV3 strongly inhibits the IFN-gamma-induced MHC class

252 nduction of MHC class I and II expression by HPIV3 suggests that it plays a role in the infection-rel

253 a level of protection against challenge with HPIV3 that was indistinguishable from that induced by pr

254 version of human parainfluenza virus type 3 (HPIV3) that is attenuated due to the presence of the bov

255 For human parainfluenza virus type 3 (HPIV3), the effects of specific mutations that alter the

256 For human parainfluenza virus type 3 (HPIV3), the receptor binding protein (hemagglutinin-neur

257 Thus, in wild-type HPIV3, the aberrant M-GE signal operates a previously un

258 hPIV1 and hPIV3 thus bind typical N-linked glycans, in contrast to

259 r to those induced by RSV infection and anti-HPIV3 titers similar to those induced by HPIV3 infection

260 V3 vector expressing RSV F as a bivalent RSV/HPIV3 vaccine and have been evaluating means to increase

261 A bivalent intranasal RSV/HPIV3 vaccine candidate consisting of a chimeric bovine/

262 yxoviruses: (i) HPIV3cp45, a live-attenuated HPIV3 vaccine candidate containing multiple attenuating

263 improved version of this well-tolerated RSV/HPIV3 vaccine candidate, with potently improved immunoge

264 e the antibody response to a live attenuated HPIV3 vaccine without affecting viral replication and at

265 gative children as a bivalent intranasal RSV/HPIV3 vaccine, and it was well tolerated but insufficien

266 creased F immunogenicity in the bivalent RSV/HPIV3 vaccine.

267 plications for the design of live attenuated HPIV3 vaccines; specifically, the antibody response agai

268 All activities of the HPIV3 variant ZM1 HN (T193I/I567V) are less sensitive to

269 We now provide evidence that the HPIV3 variant's resistance to receptor-binding inhibitio

270 sion promotion, human parainfluenza virus 3 (HPIV3) variants with alterations in HN were studied.

271 We are developing a chimeric rB/HPIV3 vector expressing RSV F as a bivalent RSV/HPIV3 va

272 The rB/HPIV3 vector expressing RSV F protein is a candidate biv

273 Each rB/HPIV3 vector induced a high titer of neutralizing antibo

274 ghtly less than, after infection with the rB/HPIV3 vector itself.

275 red immune responses against RSV G or the rB/HPIV3 vector.

276 bovine/human parainfluenza type 3 virus (rB/HPIV3) vector expressing the respiratory syncytial virus

277 d chimeric recombinant bovine/human PIV3 (rB/HPIV3) vector expressing the RSV fusion (F) glycoprotein

278 bovine/human parainfluenza virus type 3 (rB/HPIV3) vector expressing the RSV fusion F protein.

279 bovine/human parainfluenza virus type 3 (rB/HPIV3) vector to express RSV wild-type (wt) G and modifi

280 bovine/human parainfluenza virus type 3 (rB/HPIV3) vector to express various modified forms of RSV G

281 A chimeric bovine/human PIV3 (rB/HPIV3) virus expressing the unmodified, wild-type (wt) R

282 ability, we constructed and characterized rB/HPIV3 viruses expressing RSV F from the first (pre-N), s

283 est this hypothesis, two similar recombinant HPIV3 viruses from which this insert in the M-GE signal

284 nce of p53, the replication of both EMCV and HPIV3 was retarded, whereas, conversely, VSV replication

285 ma, indicating that the inhibitory effect of HPIV3 was specific to MHC class II.

286 s clinical trial in virus-naive children, rB/HPIV3 was well tolerated but the immunogenicity of wild-

287 bovine/human parainfluenza virus type 3 (rB/HPIV3) was developed previously as a vector expressing R

288 ecombinant human parainfluenza virus type 3 (HPIV3) was modified to express either the EV structural

289 e surface glycoproteins replaced by those of HPIV3, was designed to express HMPV subgroup A F protein

290 amples from patients with community-acquired HPIV3 were analyzed.

291 ntibody titers against bPIV3 and human PIV3 (hPIV3) were measured.

292 positive for HPIV2, and 9 of 10 positive for HPIV3) were positive and were correctly typed by both as

293 nize by the intranasal route against RSV and HPIV3, which are the first and second most important vir

294 ncing coverage to yield the whole genome for HPIV3, while 10 (2 cases and 8 controls) of 13 samples g

295 In contrast, coexpression of F-KDEL with HPIV3 wild-type F or the heterologous receptor-binding p

296 ading frame (ORF) of a recombinant wild-type HPIV3 with the analogous ORF from BPIV3, with the caveat

297 s thus combine the antigenic determinants of HPIV3 with the host range restriction and attenuation ph

298 us immune response to both measles virus and HPIV3, with serum antibody titers to both measles virus

299 -gamma could elicit antiviral effect against HPIV3 without cross talk with the IFN-alpha-signaling pa

300 In summary, CPD of HPIV3 yielded promising vaccine candidates suitable for