ライフサイエンスコーパス: CPV

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

2 CPV caused interstitial nephritis in six renal allograft

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

4 CPV particles colocalized with transferrin in perinuclea

5 CPV resolvase is dimer of RNase H superfamily domains re

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

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

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

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

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

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

12 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 rearranged genomes were seen in both FPV and CPV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 lymerase PCR was most effective in detecting CPV DNA.

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

53 After emerging, CPV-2 spread rapidly worldwide.

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

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

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

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

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

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

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

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

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

63 67 of 290 [23%]) or Choristoneura fumiferana CPV-16 (33 of 111 [29%]).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 injected with an infectious plasmid clone of CPV.

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

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

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

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

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

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

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

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

97 ents capturing the variable surface loops of CPV.

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

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

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

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

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

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

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

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

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

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

108 ine panleukopenia virus or a later strain of CPV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 ediate between that of Orthoreovirus and the CPV virion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 ed with the mRNA capping machinery unique to CPV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 olyhedrin of cytoplasmic polyhedrosis virus (CPV).

209 structure of Cytoplasmic polyhedrosis virus (CPV).

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

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

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

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

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

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

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

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

218 % and 49 % amino acid sequence identity with CPV and MVM, respectively, but the degree of conservatio

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

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

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

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

223 Infections with CPV and FPV showed limited genetic diversity regardless

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

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

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

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

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

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

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

231 , could be eliminated by coinfection with wt CPV.

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