ライフサイエンスコーパス: CPV

1 CPV and EPV analysis showed a considerable optical secti

2 CPV and FPV enter cells by endocytosis and can be taken

3 CPV caused interstitial nephritis in six renal allograft

4 CPV did not prevent peptide loading of MHC I but complet

5 CPV is found to be correlated with stress and also with

6 CPV particles colocalized with transferrin in perinuclea

7 CPV resolvase is dimer of RNase H superfamily domains re

8 CPV was detected in the urothelium of graft ureters, ass

9 CPV, but not the related feline parvovirus, could use re

10 CPV/49 replicates in murine hearts and pancreata, causin

11 and at one-year (CMIT: r = 0.63, p < 0.0001; CPV: r = 0.43, p = 0.004) post-transplantation along wit

12 -transplantation (CMIT: r = 0.3, p < 0.0001; CPV: r = 0.53, p = 0.009) were univariate predictors, wh

13 he donor spleen (CMIT: r = 0.73, p < 0.0001; CPV: r = 0.69, p < 0.0001) and in the donor hearts at on

14 arts at one-week (CMIT: r = 0.52, p = 0.005; CPV: r = 0.56, p = 0.002) and at one-year (CMIT: r = 0.6

15 Canine parvovirus type 2 (CPV-2) emerged as a variant of a feline parvovirus when

16 Canine parvovirus type 2 (CPV-2) emerged in 1978 and spread worldwide within 2 yea

17 Canine parvovirus type 2 (CPV-2) is a severe enteric pathogen of dogs, causing hig

18 canine parvovirus type 2c (CPV-2c) (n = 26), CPV-2b (n = 25), and CPV-2 (n = 3) were detected in the

19 ce of 54 samples, canine parvovirus type 2c (CPV-2c) (n = 26), CPV-2b (n = 25), and CPV-2 (n = 3) wer

20 tations, 43% of viruses were CPV-2a, and 57% CPV-2b, with no type 2 or 2c found.

21 The interior region of Alaska experienced a CPV outbreak in the winter of 2016 leading to the furthe

22 ion-negative rhabdomyosarcoma who harbored a CPV had outcomes comparable to patients with fusion-posi

23 ion-negative rhabdomyosarcoma who harbored a CPV had similarly inferior outcomes as patients with fus

24 The presence of a CPV in 24 rhabdomyosarcoma-associated cancer-predisposit

25 Infection of LLC-PK1 pig kidney cells with a CPV CrmA mutant, but not with wild-type (wt) CPV, result

26 t apoptosis in LLC-PK1 cells infected with a CPV recombinant deleted for CrmA but expressing Serp2.

27 % compared with 65.3% for patients without a CPV (P = .06).

28 % compared with 57.8% for patients without a CPV (P = .10), and OS was 53.7% compared with 65.3% for

29 acro- and microscale features that accompany CPV's evolutionary success.

30 pared infections that occurred shortly after CPV emerged with more recent infections and examined the

31 g monoclonal antibodies (MAb) raised against CPV was characterized.

32 Despite 40 years of viral evolution, all CPV variants are more than ~99% identical in nucleotide

33 gether, these findings suggest that although CPV is capable of rapid host adaptation, a relatively lo

34 The American CPV-2b isolates have unique codons (494 and 572) in VP2.

35 These results suggest that the RPV SPI-2 and CPV CrmA proteins are not functionally equivalent and th

36 utionary intermediates between the CPV-2 and CPV-2a strains, suggesting that passage through raccoons

37 on site in that domain bound FPV, CPV-2, and CPV-2b capsids efficiently.

38 e 2c (CPV-2c) (n = 26), CPV-2b (n = 25), and CPV-2 (n = 3) were detected in the United States.

39 olved, yet known, strains of both CPV-2a and CPV-2b were identified and grouped geographically.

40 , therefore, remarkable that both AcMNPV and CPV polyhedra possess identical crystal lattices and cry

41 of the AAV5 structure with those of ADV and CPV failed to reveal a feature which could account for t

42 The purified feline TfR inhibited FPV and CPV-2 binding and infection of feline cells but not CPV-

43 rearranged genomes were seen in both FPV and CPV.

44 ptor the expanded ability to bind to FPV and CPV.

45 )-binding site are conserved only in FPV and CPV.Our results show that the loop conformation and the

46 ediated by SPI-2 and CrmA mutants of RPV and CPV, respectively, could be eliminated by coinfection wi

47 /SPI-2) or apoptosis (myxoma virus SERP2 and CPV crmA/SPI-2), the function of other poxvirus serpins

48 not be activated by CPV-infected targets and CPV prevented the recognition of VV-infected APC upon co

49 ne the canine host range differences between CPV and feline panleukopenia virus.

50 The interaction between CPV and TfR has been extensively studied, and previous a

51 into dynamic molecular interactions between CPV and TfR.

52 into the phylogenetic relationships between CPV and other Chordopoxvirinae members we partially char

53 One antibody directed to the A site binds CPV but not FPV.

54 of newly evolved, yet known, strains of both CPV-2a and CPV-2b were identified and grouped geographic

55 This shows that both CPV-specific changes control canine TfR binding but that

56 These chimeric receptors bound CPV capsids and mediated uptake but did not result in ce

57 V turret protein (TP) is sufficient to bring CPV or engineered proteins into the polyhedrin matrix fo

58 ted human subjects could not be activated by CPV-infected targets and CPV prevented the recognition o

59 ulfide-linked complexes in varied amounts by CPV and ECT, likely enhances the dynamics of the immune

60 to define the early stages of cell entry by CPV.

61 feline TfR were susceptible to infection by CPV and FPV, but the parental TRVb cells were not.

62 ere no significant differences in outcome by CPV status of the 63 CPG set.

63 anine TfRs showed that sequences controlling CPV-specific binding were within the apical domain and t

64 lymerase PCR was most effective in detecting CPV DNA.

65 However, how polyhedrin molecules embed CPV particles inside infectious polyhedra is not known.

66 After emerging, CPV-2 spread rapidly worldwide.

67 ree-dimensional structures of full and empty CPV by electron cryomicroscopy show identical outer shel

68 report the structures of the full and empty CPV determined at 13-A resolution by electron cryomicros

69 The internal space of the empty CPV is unoccupied except for 12 mushroom-shaped densitie

70 The structure of the empty CPV reveals a density attributed to the transcription en

71 he unique active site structure observed for CPV resolvase, we have carried out a series of experimen

72 a spontaneous RNA encapsidating process for CPV assembly in vivo.

73 The amino acids required for CPV sialic acid binding map to a site at the icosahedral

74 fic structure of this region is required for CPV to retain its canine host range.

75 Cut-off values for CPV and EPV were established for fibrotic stages.

76 glycosylation site in that domain bound FPV, CPV-2, and CPV-2b capsids efficiently.

77 67 of 290 [23%]) or Choristoneura fumiferana CPV-16 (33 of 111 [29%]).

78 These findings suggest that germline CPV testing may aid in clinical prognosis and should be

79 cross-sectional study of national and global CPV phylogeographic segregation reveals a substantially

80 ace diagrams to paint a clear picture of how CPV(24h) varies for chemicals with different properties

81 Together, our results show how CPV exploits the natural mechanism of TfR endocytosis to

82 However, CPV-2 was soon replaced by a variant virus (CPV-2a) that

83 aggregates around cytopathic vacuole type I (CPV-I) structures, the absence of nucleocapsid (NC) form

84 e operational characteristics of the QD-IBSC-CPV module are a consequence of the carrier dynamics via

85 olar cell concentrator photovoltaic (QD-IBSC-CPV) module to the IEC62108 standard with recorded power

86 ated the role of cytopathic vacuole type II (CPV-II) through in situ electron tomography of alphaviru

87 In CPV the reciprocal changes of VP2 residue 93 or 323 to t

88 ent to a double Ca(2+)-binding site, both in CPV and FPV.

89 We show that the ten segmented dsRNAs in CPV are organized with ten TECs in a specific, non-symme

90 ls, and intracellular maturation of MHC I in CPV- and VV-infected human and mouse cells.

91 interactions select for escape mutations in CPV.

92 Changing both residues in CPV to the FPV amino acids blocked the canine cell infec

93 us in infection, we altered that sequence in CPV, and some of those changes made the capsids ineffici

94 During infection, CPV particles initially bound and trafficked passively o

95 ing two antibodies that recognize the intact CPV capsid into the cytoplasm of cells and also by using

96 The model was validated by comparing modeled CPV(24h) values to measured ones compiled from the liter

97 howed little similarity to Antheraea mylitta CPV-4 (67 of 290 [23%]) or Choristoneura fumiferana CPV-

98 inding and infection of feline cells but not CPV-2b, indicating that the receptor binding may be able

99 r under-vaccinated canines, not from a novel CPV strain incapable of being neutralized by current vac

100 information in terms of investigating novel CPV in this outbreak.

101 ns corresponding to surface loops 3 and 4 of CPV contain linear epitopes that are located on the exte

102 the segments that encompassed the analogs of CPV surface loops 3 and 4.

103 Western blotting analyses of CPV/49 replication in murine heart fibroblast cultures d

104 there was also up to 10-fold more binding of CPV to the surface of mutant dynamin-expressing cells th

105 Thus, the structural characteristics of CPV-II can be used in evaluating the design of a packagi

106 injected with an infectious plasmid clone of CPV.

107 High concentrations of CPV particles did not permeabilize canine A72 or mink lu

108 tates-under seven experimental conditions of CPV.

109 ly substitute for CrmA within the context of CPV and that the inhibition spectra for Serp2 and CrmA a

110 Here we show that the emergence of CPV involved an additional host range variant virus that

111 nvestigate the transmission and evolution of CPV-2 both nationally and in relation to the global situ

112 hrough raccoons assisted in the evolution of CPV-2a.

113 ons as changes observed in other isolates of CPV or feline panleukopenia virus.

114 d other countries, together with the lack of CPV-2c in this population, strongly suggests the spread

115 The location of CPV-II adjacent to the site of viral budding suggests a

116 ents capturing the variable surface loops of CPV.

117 that natural selection has channeled much of CPV evolution.

118 e host ranges, a naturally variant mutant of CPV (represented by the CPV type-2b strain) that became

119 We analyzed 12 mutants of CPV which contained amino acid changes in two adjacent l

120 There was a 40% decrease in the number of CPV-infected cells in mutant dynamin-expressing cells, a

121 The presence of CPV DNA was demonstrated in tattoos from one striped dol

122 We also evaluated the presence of CPV in skin lesions other than tattoos to examine specif

123 n, we conclude that an early gene product of CPV abrogates MHC I trafficking, thus rendering CPV-infe

124 ine cell infection is a specific property of CPV and depends on the ability of the virus to bind the

125 nging from 44.8-96.5%, and representation of CPV sequencing reads to those of the metagenome backgrou

126 population, strongly suggests the spread of CPV within its population may be heterogeneously subject

127 aptation to dogs the later variant strain of CPV gained the ability to more efficiently use the canin

128 ine panleukopenia virus or a later strain of CPV.

129 ed the structures of a variety of strains of CPV and FPV at various pH values and in the presence or

130 range, and in this study FPV and strains of CPV differed in the levels of cell attachment, uptake, a

131 ons and examined the population structure of CPV after experimental cross-species transmission to cat

132 we report the three-dimensional structure of CPV at 3.88 A resolution using single-particle cryo-elec

133 py (cryo-EM), we determined the structure of CPV in complex with Fab E to 4.1 A resolution, which all

134 ted that a region in the capsid structure of CPV, centered around VP2 position 300, varies after tran

135 ermined, as well as in two new structures of CPV capsids that contain substitutions of the VP2 Asn-93

136 blast cultures demonstrate that synthesis of CPV/49 proteins is significantly slower than that of the

137 Cross-species transmission of CPV occurs as a result of mutations on the viral capsid

138 eline transferrin receptor (TfR), while only CPV binds to the canine TfR.

139 prevented receptor binding to either FPV or CPV capsids, while replacing Leu221 with Lys resulted in

140 the altered receptors for binding to FPV or CPV capsids.

141 Canine parvovirus (CPV) and feline panleukopenia virus (FPV) are closely re

142 cesses and host ranges of canine parvovirus (CPV) and feline panleukopenia virus (FPV) are controlled

143 Canine parvovirus (CPV) and feline panleukopenia virus (FPV) capsids bind t

144 Canine parvovirus (CPV) and feline panleukopenia virus (FPV) differ in thei

145 The structures of canine parvovirus (CPV) and feline parvovirus (FPV) complexed with antibody

146 Canine parvovirus (CPV) and its relative feline panleukopenia virus (FPV) b

147 be similar to the related canine parvovirus (CPV) and minute virus of mice (MVM).

148 ce and pandemic spread of canine parvovirus (CPV) are well documented, the carnivore hosts and evolut

149 oplasmic transport of the canine parvovirus (CPV) capsid in productive infection by microinjecting tw

150 t atomic structure of the canine parvovirus (CPV) capsid revealed a 26-nm-diameter T=1 particle made

151 the association of single canine parvovirus (CPV) capsids with cellular transferrin receptors (TfR) o

152 Canine parvovirus (CPV) emerged in 1978 as a host range variant of feline p

153 Canine parvovirus (CPV) emerged in the late 1970s as a host-range variant o

154 Canine parvovirus (CPV) enters and infects cells by a dynamin-dependent, cl

155 variable surface loops of canine parvovirus (CPV) in individual fragments (pVP2b, pVP2d, pVP2e, and p

156 stitutions that eliminate canine parvovirus (CPV) infectivity and identify how those mutations change

157 Canine parvovirus (CPV) is a highly contagious pathogen that causes severe

158 Canine parvovirus (CPV) is a highly successful pathogen that has sustained

159 Canine parvovirus (CPV) is a host range variant of a feline virus that acqu

160 Canine parvovirus (CPV) is a small nonenveloped single-stranded DNA virus t

161 Canine parvovirus (CPV) is a small, nonenveloped virus that is a host range

162 Canine parvovirus (CPV) is an important pathogen causing severe diseases in

163 DNA-containing capsid of canine parvovirus (CPV) is analyzed following atomic refinement at 2.9 A re

164 nfections of animals with canine parvovirus (CPV) or its ancestor, feline panleukopenia virus (FPV).

165 Canine parvovirus (CPV) outbreaks can have a devastating effect in communit

166 Park (SNP) and, second, a canine parvovirus (CPV) route of transmission among domestic dogs living ar

167 enuation was studied in a canine parvovirus (CPV) strain grown on dog kidney cells for 115 transfers.

168 d the binding kinetics of canine parvovirus (CPV) variants isolated from raccoons-a newly recognized

169 anti-VP1-2-13 neutralized canine parvovirus (CPV) when it was incubated with the virus prior to inocu

170 a region of the capsid of canine parvovirus (CPV) which determines the ability of the virus to infect

171 hosts in the evolution of canine parvovirus (CPV), a pandemic pathogen of domestic dogs.

172 d its host range variant, canine parvovirus (CPV), can bind the feline transferrin receptor (TfR), wh

173 disease parvovirus (ADV), canine parvovirus (CPV), minute virus of mice, and bovine parvovirus, also

174 G17, tumor virus X (TVX), canine parvovirus (CPV), porcine parvovirus (PPV), rat parvovirus 1A (RPV1A

175 ia virus ("FPV-like") or canine parvovirus ("CPV-like").

176 isolates and one for the mysticete poxvirus (CPV group 2).

177 UK samples within the odontocete poxviruses (CPV group 1) and indicated that two different poxvirus l

178 of the dsRNA genome inside quiescent CPV (q-CPV) and the in situ atomic structures of TEC within CPV

179 ndergoes marked conformational change when q-CPV is converted to t-CPV, leading to formation of the R

180 ization of the dsRNA genome inside quiescent CPV (q-CPV) and the in situ atomic structures of TEC wit

181 (VP2) position 300 in the prototype raccoon CPV allows dog cell infection.

182 ts isolated from raccoons-a newly recognized CPV host-to different carnivore transferrin receptors (T

183 Notably, some position 300 residues rendered CPV noninfectious for dog, but not cat or fox, cells.

184 abrogates MHC I trafficking, thus rendering CPV-infected cells "invisible" to T cells.

185 Each individual's CPV score is computed from data collected from a repeate

186 Among the limited number of variable sites, CPV genomes exhibit complex patterns of variation that i

187 Cowpox virus Brighton red strain (CPV) contains a gene, crmD, which encodes a 320-aa tumor

188 e viruses, and an intermediate virus strain (CPV type 2) bound to higher levels on cells than did eit

189 ide replacement of the initial virus strain (CPV type 2) by a variant (CPV type 2a) characterized by

190 Subsequently, CPV-2 was completely replaced by the variant CPV-2a, whi

191 mational change when q-CPV is converted to t-CPV, leading to formation of the RNA template entry chan

192 in CPV in both quiescent and transcribing (t-CPV) states.

193 Here we report that CPV and feline panleukopenia virus (FPV), a closely rela

194 The results revealed that CPV-II contains viral glycoproteins arranged in helical

195 o infect feline cells, and here we show that CPV infects canine cells through its ability to specific

196 By using electron tomography, we show that CPV particles are occluded within the polyhedrin crystal

197 Our data suggest that CPV may utilize adhesion-strengthening mechanisms during

198 ound elsewhere in the world, suggesting that CPV VP2 has evolved a highly fit conformation.

199 The CPV(24h) increased with increasing temperature and relat

200 ediate between that of Orthoreovirus and the CPV virion.

201 ent to maintain high association between the CPV score and viral shedding, as long as the timing of t

202 ll as evolutionary intermediates between the CPV-2 and CPV-2a strains, suggesting that passage throug

203 ly variant mutant of CPV (represented by the CPV type-2b strain) that became the dominant virus world

204 rial maltose-binding proteins containing the CPV or ECT CrmD cysteine-rich region bound TNF and lymph

205 rence between these receptors determined the CPV-specific binding of the canine TfR.

206 ying molecular mechanisms, we determined the CPV-TfR interaction using cryo-electron microscopy to so

207 These regions were compared in the CPV and FPV capsid structures that have been determined,

208 tween resolvase and RuvC, and a model of the CPV resolvase.Holliday junction complex provides insight

209 e specimens demonstrated the presence of the CPV transcriptome, with read depths ranging from 2.2X -

210 n that the amino-terminal 79 residues of the CPV turret protein (TP) is sufficient to bring CPV or en

211 The X-ray crystal structure of the CPV-2a capsid shows that each mutation confers small loc

212 These data suggest that the CPV entry and infection pathway is complex and involves

213 nd previous analyses have suggested that the CPV-TfR complex is asymmetric.

214 by the tests, 6 contribute materially to the CPV score, prospectively differentiating the high from t

215 f 44% and 22% identity, respectively, to the CPV TNFR-like proteins, cytokine response modifiers (crm

216 the CPV-2a strain, while 11 belonged to the CPV-2 vaccine-derived strain.

217 n domestic dogs, 6 sequences belonged to the CPV-2a strain, while 11 belonged to the CPV-2 vaccine-de

218 Computer comparisons with the CPV crystal structure suggest that these sequences may b

219 f live feline cells and to monitor how these CPV-TfR complexes access endocytic structures.

220 nding to feline and canine cells compared to CPV type 2.

221 pervariable region (pVP2d), corresponding to CPV loop 2, was also expressed from ADV-Utah.

222 ed contained an intact crmD (97% identity to CPV crmD) and lacked cognates of crmB and crmC.

223 ys resulted in a receptor that bound only to CPV but not to FPV.

224 ed with the mRNA capping machinery unique to CPV.

225 Introducing two CPV-specific changes into FPV (at VP2 residues 93 and 32

226 The capsids of wild-type CPV and two mutants were similar in susceptibility to he

227 Unlike wild-type-CPV-infected cells, apoptosis was readily observed in ce

228 though total levels of MHC I were unchanged, CPV reduced surface levels and inhibited the intracellul

229 -exposure cognitive performance variability (CPV), defined before viral exposure occurs.

230 CPV-2 was completely replaced by the variant CPV-2a, which is characterized by four specific capsid (

231 tial virus strain (CPV type 2) by a variant (CPV type 2a) characterized by four amino acid difference

232 he crystal structure of the canarypox virus (CPV) resolvase.

233 The cowpox virus (CPV) CrmA and the equivalent rabbitpox virus (RPV) SPI-2

234 T cells of mice infected with cowpox virus (CPV) or VV recognized APC infected with VV but not APC i

235 ll virulence and, like crmA of cowpox virus (CPV), is reported to inhibit the interleukin-1beta-conve

236 analysis revealed that, unlike cowpox virus (CPV), MPV did not interfere with MHC expression or intra

237 segmented double-stranded RNA (dsRNA) virus (CPV; Reoviridae) and highlights the importance of viral

238 of purified cytoplasmic polyhedrosis virus (CPV) and that of polyhedrin protein.

239 dae members, cytoplasmic polyhedrosis virus (CPV) has a single-shelled capsid.

240 Cytoplasmic polyhedrosis virus (CPV) is unique within the Reoviridae family in having a

241 Reoviridae, cytoplasmic polyhedrosis virus (CPV) provides an attractive system for studying endogeno

242 elled insect cytoplasmic polyhedrosis virus (CPV), all package a genome of segmented double-stranded

243 olyhedrin of cytoplasmic polyhedrosis virus (CPV).

244 structure of Cytoplasmic polyhedrosis virus (CPV).

245 elled member cytoplasmic polyhedrosis virus (CPV).

246 This virus, termed cynomolgus polyoma virus (CPV), is antigenically and genomically related to simian

247 The original strain of the virus (CPV-2) emerged in dogs during the late 1970s due to a ho

248 CPV-2 was soon replaced by a variant virus (CPV-2a) that differed in antigenicity and receptor bindi

249 mation (myxoma virus SERP1 and cowpox virus [CPV] crmA/SPI-2) or apoptosis (myxoma virus SERP2 and CP

250 The chimeric virus, CPV/49, replicates like the parental CVB3 strain in HeLa

251 e 24 h cumulative percentage volatilization (CPV(24h)) loss.

252 t 24-h cumulative percentage volatilization (CPV(24h)) losses.

253 intimal thickness (CMIT) and plaque volume (CPV) by intravascular ultrasound (IVUS) examinations.

254 Collagen Proportionate Volume (CPV) and Elastin Proportionate Volume (EPV) values were

255 ey amino acid mutations, 43% of viruses were CPV-2a, and 57% CPV-2b, with no type 2 or 2c found.

256 , as FPV binds only to the feline TfR, while CPV binds to both the canine and feline TfRs.

257 % and 49 % amino acid sequence identity with CPV and MVM, respectively, but the degree of conservatio

258 In our study, LLC-PK1 cells infected with CPV delta crmA, but not those infected with wt CPV, show

259 in extracts from LLC-PK1 cells infected with CPV delta crmA, wt RPV, or RPV delta SPI-2 but not wt CP

260 Cells infected with CPV produced extremely low amounts of CrmD compared with

261 C infected with VV but not APC infected with CPV.

262 Infections with CPV and FPV showed limited genetic diversity regardless

263 A single inoculation with CPV/49 induces protective anti-CVB3 neutralizing antibod

264 e TfR controls the specific interaction with CPV capsids, as a canine TfR mutant altering a glycosyla

265 ted capsid antibodies did not interfere with CPV replication when they were coinjected with an infect

266 the in situ atomic structures of TEC within CPV in both quiescent and transcribing (t-CPV) states.

267 nfection of LLC-PK1 cells with wt RPV and wt CPV gave no PARP-cleaving activity, and all PARP cleavag

268 crmA, wt RPV, or RPV delta SPI-2 but not wt CPV.

269 V delta crmA, but not those infected with wt CPV, showed induction of poly(ADP-ribose) polymerase (PA

270 , could be eliminated by coinfection with wt CPV.

271 CPV CrmA mutant, but not with wild-type (wt) CPV, results in the induction of many of the morphologic