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 o confer bivalent protection against RSV and HPIV3.

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

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

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

9 re lower respiratory tract disease caused by HPIV3.

10 ndidate to protect against illness caused by HPIV3.

11 were protected from challenge with wild-type HPIV3.

12 e a bivalent mucosal vaccine against RSV and HPIV3.

13 tablish an effective antiviral state against 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 play an important role in the replication of HPIV3.

19 was increased for the mutants compared to wt HPIV3.

20 opment as a bivalent vaccine against RSV and HPIV3.

21 izing antibodies in hamsters against RSV and HPIV3.

22 haps other paramyxoviruses, such as hRSV and hPIV3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 nation inhibition assay was used to quantify hPIV3 antibody.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 tested resulted in complete protection from HPIV3 challenge.

67 ufficient to confer complete protection from HPIV3 challenge.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 HPIV3 F peptides were also effective in inhibiting HeV p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 ipients from developing antibody profiles of hPIV3 primary infection.

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

181 HPIV3 recombinants expressing the Ebola virus (Zaire spe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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