ライフサイエンスコーパス: SV5

1 ction with the paramyxovirus simian virus 5 (SV5).

2 ive-strand RNA paramyxovirus simian virus 5 (SV5).

3 BL/6, with the paramyxovirus simian virus 5 (SV5).

4 ot been established at d3 postinfection with SV5.

5 e of infection and expression by recombinant SV5.

6 compared to those features of wild-type (wt) SV5.

7 nfection with DC with the parental virus, WT SV5.

8 allogeneic T cells than DC infected with WT SV5.

9 esis that closely matched those seen with WT SV5.

10 taSH+MuV-SH) was analyzed in comparison with SV5.

11 amino acid differences from the F protein of SV5.

12 not from cells infected with wild-type (WT) SV5.

13 Simian virus 5 (SV5), a closely related rubulavirus, encodes a 44-amino-

14 The V protein of simian virus 5 (SV5), a prototype of the paramyxoviruses, contains a cys

15 le CD80 or CD86 above the level seen with WT SV5 alone.

16 cytopathic effect in human DC compared to WT SV5 and an enhanced ability to induce DC function has im

17 ndogenous murine IFN-alpha/beta signaling by SV5 and HPIV2 V proteins.

18 SV5 and mumps V proteins require STAT2 to recruit the ST

19 particles, and similar particles constitute SV5 and mumps VDC preparations.

20 In neutralization assays with human serum, SV5 and MuV containing CD46 showed slower kinetics and m

21 s support a model in which the rubulaviruses SV5 and MuV incorporate cell surface complement inhibito

22 s and more resistance to neutralization than SV5 and MuV that lacked CD46.

23 f MV F with those of the parainfluenza virus SV5 and Newcastle disease virus (NDV) F proteins, the st

24 have compared the outcomes of wild-type (WT) SV5 and rSV5-P/V-CPI- infections of primary human dendri

25 Comparison of SV5 and WF-PIV genome sequences revealed nine nucleotide

26 residues of CBF1 in both the simian virus 5 (SV5) and Hendra virus F proteins.

27 ons were created in both the simian virus 5 (SV5) and Hendra virus F proteins.

28 The paramyxoviruses simian virus 5 (SV5) and human parainfluenza virus 2 (HPIV2) overcome IF

29 romoted by the paramyxovirus simian virus 5 (SV5) and human parainfluenza virus type 3 (HPIV-3) fusio

30 induced cytopathic effects not seen with WT SV5, and the extent of cell killing correlated with elev

31 o CRI and CRII, optimal replication from the SV5 antigenomic promoter requires a third sequence-depen

32 Thus, optimal RNA replication from the SV5 antigenomic promoter requires three sequence-depende

33 roteins of the paramyxovirus simian virus 5 (SV5) are expressed on the surface of virus-infected cell

34 ) are much more permissive to infection with SV5 at a multiplicity of infection (MOI) of 10 PFU/cell

35 substitutions in an otherwise wild-type (WT) SV5 background.

36 The potential advantages of SV5-based oncolytic vectors are discussed.

37 ly productive infections like wild-type (WT) SV5 but that cells infected with the P/V-CPI(-) mutant s

38 related to the paramyxovirus simian virus 5 (SV5) but is defective in syncytium formation.

39 d levels of mRNA than cells infected with WT SV5, but levels of genomic RNA were not changed.

40 PI3), Sendai virus (SN), and simian virus 5 (SV5) by expression of their glycoprotein genes in HeLa T

41 productively for long periods of time; e.g., SV5 can be produced from MDBK cells for up to 40 days wi

42 cell types the paramyxovirus simian virus 5 (SV5) causes little cytopathic effect (CPE) and infection

43 ntly decreased levels of fusion, whereas the SV5 CBF(2) I49A mutant exhibited greatly increased cell-

44 MDBK cells were infected with a recombinant SV5 containing a deletion of the SH gene (rSV5DeltaSH),

45 A previously described, recombinant SV5 containing substitutions in the shared region of the

46 ' hexamers form an important sequence in the SV5 CRII promoter element.

47 The results indicated that SV5 DI RNA replication was reduced by substitutions for

48 We have previously shown, using an SV5 dicistronic minigenome, that replacement of the 22-b

49 SV5 differs from most paramyxoviruses in that it encodes

50 Our results with SV5-directed intracellular expression of flagellin may b

51 SV5 encodes eight known viral proteins, including a smal

52 ion, the model paramyxovirus simian virus 5 (SV5) establishes an infection in the respiratory tract o

53 The paramyxovirus simian virus 5 (SV5) establishes highly productive persistent infections

54 ein of MuV has a function similar to that of SV5, even though there is no sequence homology between t

55 s transfected with pCAGGS-Hendra F or pCAGGS-SV5 F (known to be proteolytically processed by furin) w

56 In contrast the SV5 F glycoprotein and the HN glycoprotein of the highly

57 Additional substitutions at SV5 F I49 suggest that both side chain volume and hydrop

58 laces the fusion and transmembrane anchor of SV5 F in close proximity with a large intervening domain

59 Deletion mutants of SV5 F indicate that putative flexible tethers between th

60 tly published prefusogenic structure of PIV5/SV5 F indicates that residues within and flanking CBF1 i

61 For some SV5 F mutants, proteolytic cleavage and surface expressi

62 fusogenic structure of parainfluenza virus 5/SV5 F places CBF(2) in direct contact with heptad repeat

63 in the initial folding and transport of the SV5 F protein and that mutations that destabilize the N-

64 was dependent on the surface density of the SV5 F protein but independent of the density of SV5 HN p

65 vious work had indicated that removal of the SV5 F protein cytoplasmic tail (F Tail- or FDelta19) cau

66 inal extents of fusion increased with rising SV5 F protein surface densities, suggesting that multipl

67 rotein was inhibited while processing of the SV5 F protein was not significantly affected.

68 partial suppression of fusion in a chimeric SV5 F protein with a CT derived from SER virus, indicati

69 t multiple fusion pores can be active during SV5 F protein-promoted membrane fusion.

70 rotein could be partially transferred to the SV5 F protein.

71 dividually to the respective residues of the SV5 F protein.

72 r amino acid differences between the SER and SV5 F proteins also play a role in regulating the fusion

73 In addition, the mutant SV5 F V402A displayed a hyperfusogenic phenotype at both

74 s transfected with pCAGGS-Hendra F or pCAGGS-SV5 F were metabolically labeled and chased in the absen

75 simian parainfluenza virus 5 fusion protein (SV5 F), revealing a 96 A long coiled coil surrounded by

76 ixing assay, it was found that the extent of SV5 F-mediated fusion was dependent on the surface densi

77 proteolytic cleavage of the simian virus 5 (SV5) F protein by the Ca(2+)-dependent protease furin, p

78 erminal heptad repeat in the simian virus 5 (SV5) F protein on protein folding, transport, and fusoge

79 od mononuclear cell-derived immature DC with SV5-flagellin resulted in enhanced levels of interleukin

80 essed from the genome of wild-type (WT) SV5 (SV5-flagellin).

81 aramyxovirus-mediated fusion, we mutated the SV5 fusion (F) protein at conserved residues L447 and I4

82 Different isolates of the paramyxovirus SV5 fusion (F) protein have either a short (20-residue)

83 Paramyxovirus SV5 fusion (F) protein-mediated fusion and its inhibitio

84 The role of the simian virus 5 (SV5) fusion (F) protein 20 residue COOH-terminal region,

85 combinations which may differentially affect SV5 gene expression and provide an additional level of t

86 ts suggest that the sequence diversity at an SV5 gene junction reflects specific combinations which m

87 (ORF) of SV5 SH with the ORF of MuV SH in a SV5 genome background.

88 plasmids containing cDNAs of the full-length SV5 genome in which the gene junction sequences (GE, IG,

89 sorting, we have investigated paramyxovirus SV5 hemagglutinin-neuraminidase (HN), a type II membrane

90 Following secondary exposure to SV5, high avidity CD8+ T cells again are the exclusive c

91 munofluorescent analysis showed internalized SV5 HN in vesicle-like structures in a juxtanuclear patt

92 F protein but independent of the density of SV5 HN protein, indicating that HN serves only a binding

93 not in mouse cells, effectively restricting SV5 host range.

94 In contrast to wild-type (WT) SV5, human cells infected with rSV5-P/V-CPI- had STAT1 l

95 l cysteine-rich domain (corresponding to the SV5 I protein) did not reduce these host cell responses

96 V5-P/V-CPI- mutant virus grew better than WT SV5 in all cell lines tested.

97 uman STAT2 can confer a growth advantage for SV5 in the murine host.

98 on pathways leading to IL-8 secretion, since SV5-infected A549 cells secreted IL-8 after stimulation

99 s of p53 and p21(CIP1) were not increased in SV5-infected cells compared to mock-infected cells, sugg

100 The SV5-infected cells had a delayed transition from G(1) to

101 The lack of IL-8 secretion from SV5-infected cells was not due to a global block in all

102 a protein (pRB) was delayed and prolonged in SV5-infected cells.

103 Immunogold staining of HN on the surface of SV5-infected CV-1 cells and examination using electron m

104 evaluated the hypothesis that activation of SV5-infected DC would be enhanced by engineering SV5 to

105 In SV5-infected Madin-Darby canine kidney (MDCK) cells, >90

106 n, as STAT1 protein could not be detected in SV5-infected MDBK cells.

107 PE) in tissue culture whereas wild-type (wt) SV5 infection does not induce CPE.

108 SV5 infection induces STAT1 degradation and IFN-alpha/be

109 (IFN-alpha/beta) signaling that occurs after SV5 infection of human cells.

110 ompared to the results seen with mock and wt SV5 infection, rSV5VDeltaC infection induced ER stress,

111 PIV5; formerly known as simian virus type 5 [SV5]) interacts with LGP2 and cooperatively inhibits ind

112 to determine the role of the simian virus 5 (SV5) intergenic regions in transcription.

113 other closely related paramyxoviruses, since SV5 is a very poor inducer of the cytokines IL-8 and MCP

114 Together, these data demonstrate that SV5 is unusual compared to other closely related paramyx

115 Simian virus 5 (SV5) is a member of the paramyxovirus family, which incl

116 The paramyxovirus simian virus 5 (SV5) is a poor activator of human dendritic cell (DC) ma

117 The parainfluenza virus simian virus 5 (SV5) is a poor inducer of innate immune responses.

118 Simian parainfluenza virus 5 (SV5) is a prototype of the Paramyxoviridae family of non

119 protein of the paramyxovirus simian virus 5 (SV5) is responsible for targeted degradation of STAT1 an

120 s that is closely related to simian virus 5 (SV5), is unusual in that it fails to induce syncytium fo

121 budding of the paramyxovirus simian virus 5 (SV5), its M protein was expressed in mammalian cells, an

122 The M-F junction differs from the other SV5 junctions by having a short M gene end U tract of on

123 Previously, it was reported that recombinant SV5 lacking the C terminus of the V protein (rSV5VDeltaC

124 Recombinant SV5 lacking the SH gene (rSV5DeltaSH) is viable and has

125 e position of the CG dinucleotide within the SV5 leader and antitrailer promoters was highly conserve

126 ed in mammalian cells, and it was found that SV5 M protein alone could not induce vesicle budding and

127 ence, as substitution of this proline in the SV5 M protein resulted in poor budding of SV5 VLPs and f

128 The SV5 matrix (M) protein lacks previously defined late dom

129 udes the inactive form iC3b, suggesting that SV5 may have mechanisms to evade the host complement sys

130 Here we show that an SV5 mutant (the P/V-CPI(-) mutant) with substitutions in

131 of these promoter variations, a recombinant SV5 mutant [Le-(U5C, A14G)] was engineered to harbor the

132 The isolation of two recombinant SV5 mutants that are defective in preventing chemokine i

133 fection following respiratory infection with SV5 or vaccinia virus.

134 protein but not in the cells expressing the SV5 P protein or the V protein lacking its unique C term

135 In contrast, a recombinant SV5 P/V gene mutant (rSV5-P/V-CPI-) overexpresses viral

136 provide proof of principle that a cytopathic SV5 P/V mutant can serve as an oncolytic virus and that

137 Our finding that the SV5 P/V mutant has both a reduced cytopathic effect in h

138 g complexes, from which efficient release of SV5 particles can occur, depends on the presence of an H

139 SV5 particles generated in CHO cells, which do not expre

140 ng the SH protein plays an important role in SV5 pathogenesis.

141 in that expresses fibrocystin along with two SV5-Pk epitope tags engineered in-frame into the third e

142 se is not a important factor modulating the SV5 polymerase activity.

143 Our results support a model whereby the SV5 promoter has evolved to function at an attenuated le

144 paramxyovirus simian parainfluenza virus 5 (SV5) promotes virus-cell and cell-cell membrane fusion.

145 PE compared to cells infected with wild-type SV5 (recovered from cDNA; rSV5).

146 omoter for the paramyxovirus simian virus 5 (SV5) requires two essential and discontinuous elements:

147 paramyxovirus simian parainfluenza virus 5 (SV5) resulted in mutant F proteins with hyperactive fusi

148 A recombinant SV5 (rSV5-P/V-CPI-) was engineered to contain six natura

149 The recombinant SV5 (rSV5DeltaSH+MuV-SH) was analyzed in comparison with

150 By constructing a chimeric SV5-SER virus F CT protein, we also found that the inhib

151 ed mutant, L539,548A, as well as by chimeric SV5/SER F proteins was also dramatic.

152 Furthermore, both ectopically expressed SV5 SH and MuV SH blocked activation of NF-kappaB by TNF

153 V5DeltaSH-induced apoptosis, suggesting that SV5 SH plays an essential role in blocking the TNF-alpha

154 ave replaced the open reading frame (ORF) of SV5 SH with the ORF of MuV SH in a SV5 genome background

155 hat MuV SH has a function similar to that of SV5 SH.

156 with the parainfluenza virus simian virus 5 (SV5) show minimal activation of host cell interferon (IF

157 cells infected with rSV5-P/V-CPI- but not WT SV5 showed an activation of a reporter gene that was und

158 ct cell cycle progression, and we found that SV5 slows the rate of proliferation of HeLa T4 cells.

159 MuV-SH was viable and behaved like wild-type SV5, suggesting that MuV SH has a function similar to th

160 expressed from the genome of wild-type (WT) SV5 (SV5-flagellin).

161 Simian virus 5 (SV5) targets STAT1, human parainfluenza virus 2 targets

162 We show here for the paramyxovirus SV5 that proteasome inhibitors and expression of dominan

163 lyzed the growth properties of a recombinant SV5 that was engineered to be defective in targeting STA

164 shown for the paramyxovirus simian virus 5 (SV5) that a functional promoter for RNA replication requ

165 mutant of the paramyxovirus simian virus 5 (SV5) that harbors mutations in the P/V gene from the can

166 e particularly important for viruses such as SV5, that express a V protein targeting mda-5 but do not

167 For the paramyxovirus simian virus 5 (SV5), the cytoplasmic tail of the hemagglutinin-neuramin

168 Unlike WT SV5, the Le-(U5C, A14G) mutant was a potent inducer of i

169 identification of mechanisms utilized by WT SV5 to avoid activation of host cell innate immune respo

170 infected DC would be enhanced by engineering SV5 to express a Toll-like-receptor (TLR) ligand.

171 paramyxovirus simian parainfluenza virus 5 (SV5) to affect cell cycle progression, and we found that

172 with the model paramyxovirus simian virus 5 (SV5) to study CD8+ T-cell responses in the lung.

173 e were also observed in cells expressing the SV5 V protein but not in the cells expressing the SV5 P

174 Our results confirm a role for the SV5 V protein in blocking IFN signaling but also suggest

175 Purified SV5 V protein spontaneously assembles into spherical mac

176 By contrast, an SV5 variant isolated from persistently infected cells (W

177 In contrast, the naturally occurring SV5 variant Wake Forest parainfluenza virus (WF-PIV) act

178 estern blot analysis indicated that purified SV5 virions derived from human A549 cells contained CD46

179 h purified complement components showed that SV5 virions had C3b cofactor activity, resulting in spec

180 In comparison with C3b, purified SV5 virions had very low cofactor activity against C4b,

181 cells had higher C4b cofactor activity than SV5 virions.

182 dding of SV5 VLPs and failure of recombinant SV5 virus to replicate normally.

183 ndistinguishable from those of the wild-type SV5 virus.

184 he SV5 M protein resulted in poor budding of SV5 VLPs and failure of recombinant SV5 virus to replica

185 G3A and G7A mutations into the F proteins of SV5 (W3A and WR isolates), Newcastle disease virus (NDV)

186 WT SV5 was a poor activator of the eIF-2alpha kinase protei

187 cells infected with rSV5-P/V-CPI- but not WT SV5 was confirmed by a bioassay for IFN.

188 The unique C terminus of the V protein of SV5 was shown previously to interact with DDB1, which is

189 the requirements for assembly and budding of SV5, we generated two double-mutant recombinant viruses

190 Because MuV is closely related to SV5, we hypothesize that the SH protein of MuV has a fun

191 noncytopathic paramyxovirus simian virus 5 (SV5), which is a poor inducer of host cell responses, in

192 eatment of the paramyxovirus simian virus 5 (SV5) with human serum results in deposition of complemen

193 ung A549 cells infected with simian virus 5 (SV5) with other members of the Rubulavirus genus of para

194 SV5 without the SH gene (rSV5deltaSH) is viable, and gro

195 The G3A and G7A mutations cause SV5 WR F, but not NDV F or HPIV3 F, to be triggered to c