ライフサイエンスコーパス: PRV

1 PRV and both MVM strains generated more modest lytic eff

2 PRV Bartha infection of a limited number of retinorecipi

3 PRV Bartha is not impaired in retrograde axonal transpor

4 PRV Bartha is thus a retrograde transsynaptic marker in

5 PRV capsid structures closely resemble those of HSV-1, i

6 PRV G9P[13] induced longer rectal virus shedding and RV

7 PRV immunohistochemistry combined with ISH for both GlyT

8 PRV immunoreactive fibers/cells were not altered by neon

9 PRV injections into homeostatic effector organs invariab

10 PRV injections into the NAc core yielded greater numbers

11 PRV is capable of infecting and killing a wide variety o

12 PRV virions contain a double-stranded DNA genome within

13 PRV-152, a strain that expresses enhanced green fluoresc

14 PRV-152, a strain that expresses enhanced green fluoresc

15 PRV-152, a strain that expresses enhanced green fluoresc

16 PRV-Ba transneuronal retrograde labeling revealed that c

17 expression of the polycythemia rubra vera-1 (PRV-1) gene in polycythemia vera (PV) but not in seconda

18 A PRV mutant lacking pUL25 does not produce C-capsids and

19 A PRV strain expressing the green fluorescent protein (PRV

20 We observed that both wild-type virus and a PRV gD null mutant are capable of spreading from axons t

21 We also constructed a PRV recombinant that expresses a functional gE-GFP fusio

22 eplace PRV Us9 when they were expressed in a PRV background.

23 We constructed UL54 null mutations in a PRV bacterial artificial chromosome using sugar suicide

24 usly constructed and characterized PRV152, a PRV-Bartha derivative that expresses the enhanced green

25 ization, and application of strain PRV614, a PRV-Bartha derivative expressing a novel monomeric red f

26 Using a PRV strain expressing a fluorescent capsid and a fluores

27 In addition, PRV-labeled neurons or axons were immunopositive for GAB

28 exhibited aberrant electrical activity after PRV infection due to the action of viral membrane fusion

29 (1) by removing the infected eye 24 hr after PRV 152 inoculation, well before viral infection first a

30 P[8] induced only partial protection against PRV challenge.

31 Occupancy of CVSC on all PRV capsids is near 100%, compared to ~50% reported for

32 Moreover, the HSV-1 and PRV gDs compete for binding to nectin-1.

33 atrin 3 was also phosphorylated by HSV-1 and PRV in a US3 kinase-dependent manner and by VZV ORF66 ki

34 following entry demonstrates that HSV-1 and PRV share a conserved mechanism for postentry retrograde

35 of cells that could be infected by HSV-1 and PRV were enhanced by calcium depletion.

36 The BHV-1, EHV-1, and PRV proteins complement ICP0-null mutant HSV-1 plaque fo

37 ontralesional rewiring measured with BDA and PRV tracing was related to sensorimotor dysfunction.

38 Both the CTbeta and PRV injections also resulted in labeling of neurons in a

39 rity of identified contacts between DbH- and PRV-positive profiles were classified as close appositio

40 dentified synaptic contacts between DbH- and PRV-positive profiles were classified as symmetric (Gray

41 HSV and PRV capsid-associated particles with bound green fluores

42 microscopy revealed that binding of HSV and PRV gD was localized to adherens junctions in cells main

43 At the same time, HSV and PRV homologs cannot be swapped, which suggests that in a

44 Moreover, the binding sites for HSV and PRV or BHV-1 gDs on nectin-1 may overlap but are not ide

45 lutamine [Q]) reduced the ability of HSV and PRV particles to subsequently traffic along microtubules

46 Chimeric gD molecules composed of HSV and PRV sequences can substitute, provided the first 285 aa

47 ms of viral gD and to be infected by HSV and PRV, before and after calcium depletion.

48 VP26, the small capsid protein of HSV and PRV, was one of the first herpesvirus proteins to be fus

49 ificant differences between monosynaptic and PRV cases in the subnuclear distribution or proportions

50 increases the plaquing efficiency of VZV and PRV lacking US3 or its enzymatic activity, whereas only

51 h wild-type viruses, suggesting that VZV and PRV US3 kinase activities target HDACs to reduce viral g

52 HSV-1, VZV, and PRV induced very different substrate profiles that were

53 We refer to this new method as PRV-Circuit-TRAP (PRV circuit-directed TRAP).

54 strains of pseudorabies virus (PRV), such as PRV Bartha, are among the most popular virus circuit tra

55 observed after infections with an attenuated PRV recombinant used for circuit tracing or with PRV mut

56 ontrast, animals infected with an attenuated PRV vaccine strain (PRV-Bartha) survive approximately th

57 ne of three selected virulent and attenuated PRV strains.

58 a recombinant of pseudorabies virus Bartha (PRV) into the contralateral vestibular nuclei.

59 transport of the pseudorabies virus Bartha (PRV-Bartha) strain has become an important neuroanatomic

60 ce infected with virulent (e.g., PRV-Becker, PRV-Kaplan, or PRV-NIA3) strains self-mutilate their fla

61 axodendritic and axosomatic contacts between PRV-labeled afferents and LC neurons labeled with tyrosi

62 Brainstem neurons coinfected with both PRV recombinants, which presumably had collateralized pr

63 cating that hyperphosphorylation of HDAC2 by PRV occurs in a US3-independent manner.

64 as an experimental approach to characterize PRV recombinants in general are also discussed.

65 cted into the NAc in rats and after 3-4 days PRV-infected HSD2 neurons were identified.

66 Following survival times >/=3 days, PRV-infected neurons were additionally present in nucleu

67 irus (PRV) infection of the rat retina: does PRV egress solely from axon terminals, or can the virus

68 Transneuronal retrograde dual PRV labeling has the potential to be a powerful addition

69 During PRV infection, glycoprotein B (gB)-dependent fusion even

70 on of axonal mRNAs is required for efficient PRV retrograde transport and infection of cell bodies.

71 that structural requirements for HSV entry, PRV and BHV-1 entry, and homotypic and heterotypic trans

72 btain equivalent infection were established, PRV-152 and BaBlu were injected into the left and right

73 tin microtubule motor complex as well as for PRV virulence and retrograde axon transport in vivo.

74 fit, suggesting either a different fold for PRV pUL25 or a capsid-bound conformation for pUL25 that

75 ies virus tegument, VP22 is not required for PRV replication, virulence, or neuroinvasion.

76 from the nucleus of infected cells and from PRV virions was determined by cryo-electron microscopy (

77 hasone (Dex) to protect chicken embryos from PRV-induced brain damage.

78 reported structure of the UL37 homolog from PRV, provides a much needed 3-dimensional template for t

79 of the N-terminal half of UL37 (UL37N) from PRV.

80 Mice infected with virulent (e.g., PRV-Becker, PRV-Kaplan, or PRV-NIA3) strains self-mutila

81 t protein expressing pseudorabies virus (GFP-PRV) to (1) characterize age-dependent changes in the ex

82 nt erythroid colonies (EECs) and granulocyte PRV-1 mRNA levels to discriminate polycythemias and thro

83 d 4 of 12 with ET, and increased granulocyte PRV-1 mRNA levels were found in 9 of 13 patients with PV

84 ools of low PRV countries than those of high PRV countries.

85 er overall nucleotide identity with historic PRV strains.

86 have been studied, little is known about how PRV evades the IFN-mediated immune response.

87 However, PRV does not infect humans.

88 ells to infection by G9 and other common HRV/PRV genotypes.

89 injected into the BAT of mice, we identified PRV-labeled LepRb neurons in the DMH/DHA and mPOA (and o

90 orylation of STAT1, became less effective in PRV-infected cells.

91 ough a suppression of cytokine expression in PRV-induced inflammation, which results from NF-kappaB i

92 152 revealed the presence of burst-firing in PRV-infected lamina I neurons, thereby confirming that p

93 genetic data, indicate that the mutations in PRV Bartha render the virus incapable of anterograde tra

94 NO, IL-1beta, IL-6, and MCP-1 production in PRV-infected RAW264.7 cells.

95 clooxygenases caused a dramatic reduction in PRV growth.

96 young age in 2003, could not have influenced PRV in 2003.

97 retrograde labeling following intrachoroidal PRV injection to identify central neuronal cell groups i

98 amining central infection after intravitreal PRV 152 injection in animals with ablation of the EW.

99 esty is stronger in the subject pools of low PRV countries than those of high PRV countries.

100 analyse the kinetic properties of the lytic PRV transcripts and to then classify them accordingly.

101 Moreover, PRV G9P[13] replicated more extensively in porcine monoc

102 The gD-positive and gD-negative PRV capsids were both capable of trafficking along micro

103 ortion of patients with increased neutrophil PRV-1 expression was 83% in PV, 21% in ET, 42% in MMM, 1

104 The value of quantization of neutrophil PRV-1 mRNA, platelet c-mpl expression, in vitro assays o

105 However, quantifying neutrophil PRV-1 mRNA, while complementary to other tests, is not i

106 We conclude that neutrophil PRV-1 up-regulation is a characteristic feature of PV th

107 During a gE-null PRV infection, a subset of viral glycoproteins, capsids,

108 n blotting in isolated axons during Us9-null PRV infection.

109 Within the NTS 28.5+/-9.4% of PRV-positive neurons contained LepRb-GFP, while in the R

110 ned LepRb-GFP, while in the RCH 37+/-1.7% of PRV neurons also contained LepRb.

111 Over 90% of PRV-152 labeled neurons were also labeled subsequent to

112 We took advantage of PRV gD mutants that are not infectious as extracellular

113 Based on analysis of PRV-Bartha infection density, we demonstrate two paralle

114 A striking characteristic of PRV infection is the different symptoms and outcomes of

115 Both classes of PRV particle bound to microtubules in vitro with compara

116 s with dendritic and somatic compartments of PRV-positive neurons, although dendrites were contacted

117 detailed understanding of the composition of PRV virions has been lacking.

118 teractions of nectin-2 impaired the entry of PRV and BHV-1 when introduced into either nectin-1 or ne

119 nd HSV-2 gDs but did not impair the entry of PRV and BHV-1.

120 log, mouse nectin-2, which mediates entry of PRV but not HSV-1 or HSV-2.

121 V-1 and HSV-2 entry but not for the entry of PRV or BHV-1.

122 e induction in the replication and growth of PRV.

123 se in primary cells from the natural host of PRV but is not necessary in nonnatural-host cells.

124 Adult pigs, the natural hosts of PRV, survive infection with only mild respiratory sympto

125 SCN indicate that intravitreal injection of PRV Bartha produces a retrograde infection of the autono

126 s9 homologs could compensate for the loss of PRV Us9 in anterograde, neuron-to-cell spread of infecti

127 ere able to fully compensate for the loss of PRV Us9, whereas VZV and HSV-1 Us9 proteins were unable

128 degranulation and NK cell-mediated lysis of PRV- or HSV-2-infected cells.

129 a54 is highly attenuated in a mouse model of PRV infection.

130 into the NAc core yielded greater numbers of PRV-labeled HSD2 neurons than did comparable injections

131 associated with the presently used pairs of PRV recombinants.

132 We suggest that prenylation of PRV Us2 protein is required for proper membrane associat

133 ual tracing, the neuroinvasive properties of PRV-152 and BaBlu were characterized by conducting param

134 A reconstruction of PRV capsids in which green fluorescent protein was fused

135 ting the efficient growth and replication of PRV in primary cells.

136 e transneuronal transport and replication of PRV were distributed throughout the spinal cord, but wer

137 ed culture system to investigate the role of PRV Us3 in viral replication in neurons, in spread from

138 howed that the retrograde-directed spread of PRV Bartha is slower than that of wild-type PRV.

139 Additionally, neuron-to-cell spread of PRV most likely does not proceed through syncytial conne

140 required for efficient growth and spread of PRV, indicating that altered mitochondrial transport enh

141 ent report that used a recombinant strain of PRV Bartha (PRV152) expressing enhanced green fluorescen

142 eal inoculation with a recombinant strain of PRV Bartha constructed to express enhanced green fluores

143 r, the present use of recombinant strains of PRV expressing different reporters that are driven by di

144 troduced by employing recombinant strains of PRV-Bartha engineered to express different reporter prot

145 rting HSV-1 is remarkably similar to that of PRV.

146 ynamics were indistinguishable from those of PRV and did not differ in neurons of human, mouse, or av

147 promotes retrograde microtubule transport of PRV capsids.

148 Meanwhile, the influence of beta-carotene on PRV-induced inflammation was also investigated.

149 blasts for neuron-to-cell spread of HSV-1 or PRV infection.

150 cells transiently expressing either HSV-1 or PRV proteins.

151 ge cells infected with US3-negative HSV-1 or PRV.

152 ss-protection in pigs challenged with HRV or PRV, whereas HRV Wa G1P[8] induced only partial protecti

153 h virulent (e.g., PRV-Becker, PRV-Kaplan, or PRV-NIA3) strains self-mutilate their flank skin in resp

154 ypothalamic area (LHA) significantly overlap PRV and the physiological glucose-sensing enzyme glucoki

155 express enhanced green fluorescent protein (PRV 152).

156 in expressing the green fluorescent protein (PRV-152) was injected into the left gastrocnemius muscle

157 ck infected or infected with either purified PRV-Becker or HSV-1(F).

158 nsive proteomic characterization of purified PRV virions by mass spectrometry using two complementary

159 a dual-color system by growing a recombinant PRV expressing a red fluorescent VP26 fusion (PRV180) on

160 Here, we describe a new recombinant PRV expressing a carboxy-terminal VP26-mCherry fusion.

161 mpathectomized, whereas another recombinant (PRV-BaBlu) was injected into the left adrenal gland.

162 proteins were unable to functionally replace PRV Us9 when they were expressed in a PRV background.

163 ison of the CVSC density in a 9-A-resolution PRV C-capsid map with the available crystal structure of

164 ely assessed the pathogenesis of porcine RV (PRV) G9P[13] and evaluated the short-term cross-protecti

165 ous observations in the rat, muscle-specific PRV injection lead to labeling within multiple areas of

166 using the pseudorabies virus-Bartha strain (PRV-Bartha) tracer in the rat to examine both direct (fi

167 ected with an attenuated PRV vaccine strain (PRV-Bartha) survive approximately three times longer tha

168 following injection of the parental strain, PRV-Bartha, into the left kidney.

169 tracing using isogenic recombinant strains (PRV-152 and BaBlu) of pseudorabies virus.

170 Thus, VP1/2 tethers PRV capsids to dynein/dynactin to enhance microtubule tr

171 Complete genome sequencing demonstrated that PRV G9P[13] possessed a human-like G9 VP7 genotype but s

172 try and shows no overlap, demonstrating that PRV transmission is confined to synaptically connected n

173 We discovered that PRV infection could spread efficiently from neurons to c

174 on infection from cell bodies, we found that PRV infection induces local protein synthesis in axons,

175 We show here that PRV gD, when coexpressed with HSV gB, gH, and gL, cannot

176 We show that PRV and herpes simplex virus type 1 (HSV-1) infection of

177 imbic dopamine pathway and further show that PRV circuit-directed translating ribosome affinity purif

178 Previous studies have shown that PRV glycoprotein B (gB), a component of the viral fusion

179 h PRV but not CTB, a pattern suggesting that PRV entered NSC-derived neurons via transneuronal transf

180 The PRV capsid imaged within virions closely resembles C-cap

181 The PRV protein Us9 plays an essential but unknown role in a

182 The PRV Us9 protein copurifies with KIF1A, recruiting the mo

183 gnificant structure conservation between the PRV and HSV capsids.

184 dissemination and relative virulence of the PRV strains.

185 esulted in Cre-mediated recombination of the PRV-263 genome and conditional expression of cyan/yellow

186 Here, we show that the PRV EP0 protein is necessary to overcome an interferon-m

187 Therefore, PRV was used to infect murine macrophages (RAW264.7 cell

188 Akin to PRV Us9, all of the Us9 homologs localized to the trans-

189 irectly to virus injection sites, similar to PRV.

190 ns that expressed EGFP 60-72 h subsequent to PRV-152 inoculation of vagal terminals in the stomach wa

191 e-labeled with a trans-neural, viral tracer (PRV-152).

192 tative analyses of primary and transsynaptic PRV immunolabeling confirmed an age-dependent assembly o

193 efer to this new method as PRV-Circuit-TRAP (PRV circuit-directed TRAP).

194 The wild-type PRV Becker strain spreads efficiently to postsynaptic ne

195 In this study, we determined if wild-type PRV infection can overcome the establishment of a beta i

196 arlier time until death induced by wild-type PRV infection may reflect the peripheral nervous system

197 ere simultaneously infected with a wild-type PRV strain.

198 roximately three times longer than wild-type PRV-infected animals, exhibit severe CNS abnormalities,

199 PRV Bartha is slower than that of wild-type PRV.

200 for understanding the mechanisms underlying PRV entry, assembly, egress, spread, and pathogenesis.

201 Unexpectedly, PRV infection can also spread transneuronally via axo-ax

202 Unlike PRV, however, H129 was not transported transneuronally i

203 We also found that unlike PRV gD, HSV-1 gD is required for neuron-to-cell spread o

204 We used PRV-263 in combination with a unique lentivirus vector t

205 ndex of the 'prevalence of rule violations' (PRV) based on country-level data from the year 2003 of c

206 e viral fusion proteins produced by virulent PRV infection induce electrical coupling in unmyelinated

207 nation for the uniform lethality of virulent PRV infection of nonnatural hosts.

208 Infection with virulent PRV caused these PNS neurons to fire synchronously and c

209 s with the trans-synaptic pseudorabies virus PRV-152 revealed the presence of burst-firing in PRV-inf

210 the attenuated strain of pseudorabies virus (PRV Bartha) results in transneuronal spread of virus to

211 of the Bartha strain of pseudorabies virus (PRV Bartha) results in transsynaptic infection of the hy

212 al herpesviruses porcine pseudorabies virus (PRV) and bovine herpesvirus 1 (BHV-1).

213 used method to visualize pseudorabies virus (PRV) and herpes simplex virus (HSV) particles in living

214 f the alphaherpesviruses pseudorabies virus (PRV) and herpes simplex virus 2 (HSV-2) displays previou

215 Pseudorabies virus (PRV) and herpes simplex virus type 1 (HSV-1) are distant

216 Both Pseudorabies virus (PRV) and human Herpes simplex virus (HSV) are DNA viruse

217 virus type 1 (HSV-1) and pseudorabies virus (PRV) and ORF66 in varicella-zoster virus (VZV), affects

218 The structure of pseudorabies virus (PRV) capsids isolated from the nucleus of infected cells

219 combinant strains of the pseudorabies virus (PRV) for trans-synaptic tract tracing.

220 combinant strains of the pseudorabies virus (PRV) for transsynaptic tract-tracing.

221 combinant strains of the pseudorabies virus (PRV) for transsynaptic tract-tracing.

222 ansneuronal transport of pseudorabies virus (PRV) from the stomach wall.

223 Pseudorabies virus (PRV) glycoprotein E (gE) is a type I viral membrane prot

224 uronal retrograde tracer pseudorabies virus (PRV) in rats, we previously localized preganglionic neur

225 axonal assemblies after pseudorabies virus (PRV) infection of cultured neurons.

226 sion profile after acute pseudorabies virus (PRV) infection of the CNS using Affymetrix GeneChip tech

227 ss from neurons by using pseudorabies virus (PRV) infection of the rat retina: does PRV egress solely

228 simplex virus (HSV) and pseudorabies virus (PRV) infection, a culture system consisting of sympathet

229 simplex virus type 1 and pseudorabies virus (PRV) infections of rat embryonic fibroblast (REF) cells.

230 ns-synaptic migration of pseudorabies virus (PRV) injected into the adrenal gland.

231 de, transsynaptic tracer pseudorabies virus (PRV) injected into the BAT of mice, we identified PRV-la

232 retrograde transport of pseudorabies virus (PRV) injected into the kidneys of rats.

233 phaherpesviruses such as pseudorabies virus (PRV) invade axons of peripheral nervous system neurons a

234 Pseudorabies virus (PRV) is a broad host range, swine alpha herpesvirus that

235 Transneuronal spread of pseudorabies virus (PRV) is a multistep process that requires several virall

236 Pseudorabies virus (PRV) is a useful tracer that is retrogradely and transyn

237 Pseudorabies virus (PRV) is an alphaherpesvirus related to the human pathoge

238 Pseudorabies virus (PRV) mutants lacking the Us9 gene cannot spread from pre

239 entry activity, but not pseudorabies virus (PRV) or bovine herpesvirus 1 (BHV-1) entry, did not redu

240 nsneuronal tracer Bartha-pseudorabies virus (PRV) or the retrograde marker cholera toxin B (CTB) into

241 we refine this map using pseudorabies virus (PRV) retrograde tracing, indicating that the pancreatic

242 The attenuated pseudorabies virus (PRV) strain Bartha contains several characterized mutati

243 njection of the virulent pseudorabies virus (PRV) strain Becker into late-stage chicken embryos, the

244 his, we have constructed pseudorabies virus (PRV) strains in which viral propagation and fluorophore

245 e lytic transcriptome of pseudorabies virus (PRV) throughout a 12-hour interval of productive infecti

246 y immunogold labeling of pseudorabies virus (PRV) transported retrogradely and transneuronally from i

247 The pseudorabies virus (PRV) UL54 homologs are important multifunctional protein

248 emonstrate here that the pseudorabies virus (PRV) Us2 protein is synthesized early after infection an

249 The pseudorabies virus (PRV) Us3 gene is conserved among the alphaherpesviruses

250 Pseudorabies virus (PRV) Us9 is a small, tail-anchored (TA) membrane protein

251 ) and, as reported here, pseudorabies virus (PRV) utilize the ESCRT apparatus to drive cytoplasmic en

252 sport of fully assembled pseudorabies virus (PRV) virions is dependent on the viral protein Us9.

253 ade transneuronal tracer pseudorabies virus (PRV) was microinjected into the CEAm or MEAad.

254 Pseudorabies virus (PRV), a broad host range alphaherpesvirus, causes violen

255 Pseudorabies virus (PRV), a member of the Alphaherpesvirinae, has a complex

256 is (VSV), Sindbis virus, pseudorabies virus (PRV), adeno-associated virus (AAV), and minute virus of

257 Using pseudorabies virus (PRV), an alphaherpesvirus capable of transneuronal sprea

258 Pseudorabies virus (PRV), an alphaherpesvirus related to herpes simplex viru

259 howed that proteins from pseudorabies virus (PRV), an alphaherpesvirus, localize to mitochondria and

260 pesvirus type 1 (EHV-1), pseudorabies virus (PRV), and varicella-zoster virus (VZV) and their subsequ

261 herpes simplex virus and pseudorabies virus (PRV), are neuroinvasive dsDNA viruses that establish lif

262 ated animal herpesvirus, pseudorabies virus (PRV), encodes a homologous set of glycoproteins and its

263 plex virus 1 (HSV-1) and pseudorabies virus (PRV), have suggested that UL37 plays an essential albeit

264 ed to colloidal gold, or pseudorabies virus (PRV), into the nuclear core of the rat LC.

265 herpesviruses, including pseudorabies virus (PRV), spread directionally within the nervous systems of

266 uated vaccine strains of pseudorabies virus (PRV), such as PRV Bartha, are among the most popular vir

267 HSV-2, and veterinarian pseudorabies virus (PRV), that infect the peripheral nervous system and have

268 nsneuronal viral tracer, pseudorabies virus (PRV), was injected into the ventral stomach wall in inta

269 nsneuronal tract tracer, pseudorabies virus (PRV), we also tested whether the components of these cir

270 Using pseudorabies virus (PRV), we have previously shown that the 62 carboxy-termi

271 uroinvasive herpesvirus, pseudorabies virus (PRV), we show that the viral protein 1/2 (VP1/2) tegumen

272 on of an mRFP-expressing pseudorabies virus (PRV), which acts as a transsynaptic retrograde tracer.

273 Pseudorabies virus (PRV)-a retrograde transneuronal tracer-was injected into

274 aherpesviruses-including pseudorabies virus (PRV)-use retrograde axonal transport to travel toward th

275 a-zoster virus (VZV) and pseudorabies virus (PRV).

276 herpesviruses: HSV-1 and pseudorabies virus (PRV).

277 nd attenuated strains of pseudorabies virus (PRV).

278 g recombinant strains of pseudorabies virus (PRV).

279 implex viruses (HSV) and pseudorabies virus (PRV).

280 tracing with fluorescent pseudorabies virus (PRV).

281 tion-competent strain of pseudorabies virus (PRV-263) that changes the profile of fluorescent reporte

282 ade transneuronal tracer pseudorabies virus (PRV-Ba) was injected into rat choroid, and immunolabelin

283 oblastoma in an in vivo mouse model, whereas PRV and AAV remained at the injection site with minimal

284 mpathectomized gastrocnemius muscle, whereas PRV-BaBlu, which expresses beta-galactosidase, was injec

285 mpathectomized gastrocnemius muscle, whereas PRV-BaBlu, which expresses beta-galactosidase, was injec

286 a both afferent and efferent routes, whereas PRV-Bartha travels by only efferent routes in the PNS en

287 However, the only areas in which PRV and LepRb colocalization was detected were within th

288 results support an assembly process in which PRV capsids acquire a membrane in the cell body prior to

289 sympathectomized gastrocnemius muscle, while PRV-BaBlu, which expresses beta-galactosidase, was injec

290 identified 47 viral proteins associated with PRV virions, 40 of which were previously localized to th

291 identified 48 host proteins associated with PRV virions, many of which have known functions in impor

292 uctures in the nuclei of cells infected with PRV in the presence of a COX-1/2 inhibitor.

293 o hyperphosphorylated in cells infected with PRV lacking US3 kinase, indicating that hyperphosphoryla

294 tonomic ganglia in living mice infected with PRV strains expressing GCaMP3, a genetically encoded cal

295 he estrous cycle after cervix injection with PRV; (2) in contrast, the number of infected neurons in

296 acing, NSC-derived neurons were labeled with PRV but not CTB, a pattern suggesting that PRV entered N

297 spinal cord, nNOS neurons co-localized with PRV-infected cells in the dorsal horn in laminae I, III-

298 se Cre-expressing catecholamine neurons with PRV-263 resulted in Cre-mediated recombination of the PR

299 recombinant used for circuit tracing or with PRV mutants lacking either viral glycoprotein B, require

300 All 5 MMM patients with PRV-1 up-regulation had an antecedent history of PV.