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 capsid structures closely resemble those of HSV-1, i

5 PRV causes neurological, respiratory, and reproductive d

6 PRV entry into several cell lines, including porcine kid

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

8 PRV immunohistochemistry combined with ISH for both GlyT

9 PRV immunoreactive fibers/cells were not altered by neon

10 PRV injections into homeostatic effector organs invariab

11 PRV injections into the NAc core yielded greater numbers

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

13 PRV virions contain a double-stranded DNA genome within

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

20 characterize the underlying mechanisms for a PRV-induced, accelerated degradation of KIF1A, a kinesin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Data from both HSV1 and PRV laboratories have identified a Rab6 secretory pathwa

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

43 = 0.37; p = 0.14, respectively, for PRF and PRV) or RV end-systolic volume (r = 0.2; p = 0.42 and r

44 = 0.19; p = 0.45, respectively, for PRF and PRV).

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

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

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

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

49 nal sorting and transport of newly assembled PRV virions.

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

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

52 ne of three selected virulent and attenuated PRV strains.

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

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

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

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

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

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

59 tanding the molecular mechanisms utilized by PRV to enter host cells is an important step in identify

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

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

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

63 Here, we demonstrate PRV entry into multiple model cell lines via a low-pH en

64 Dual PRV-labeled cells were found in parvocellular, magnocell

65 However, dual PRV-labeled cells in PVN only occasionally expressed OX

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

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

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

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

70 osomal pH is an important route of entry for PRV.IMPORTANCE PRV is a pathogen of great economic and a

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

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

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

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

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

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

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

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

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

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

81 er overall nucleotide identity with historic PRV strains.

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

83 However, PRV does not infect humans.

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

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

86 V) RNA G-quadruplex and ligand complex, (ii) PRV DNA G-quadruplex, and (iii) an i-motif of human telo

87 important route of entry for PRV.IMPORTANCE PRV is a pathogen of great economic and animal welfare i

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

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

90 152 revealed the presence of burst-firing in PRV-infected lamina I neurons, thereby confirming that p

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

92 clooxygenases caused a dramatic reduction in PRV growth.

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

94 of cellular acid sphingomyelinase inhibited PRV entry.

95 Interestingly, PRV infection of neuronal cells leads not only to a nons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 Exposure of PRV virions to pH 5.0 in the absence of host cell membra

116 e induction in the replication and growth of PRV.

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Using a series of PRV mutants deficient in axonal sorting and anterograde

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

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

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

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

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

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

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

138 promotes retrograde microtubule transport of PRV capsids.

139 motor promoting the sorting and transport of PRV virions in axons.

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

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

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

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

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

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

146 nt correlations were observed between PRF or PRV and RV ejection fraction (r = -0.04; p = 0.87 and r

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

148 y treatment with hypertonic medium prevented PRV entry.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 We show that PRV infection disrupts the synthesis of KIF1A and simult

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

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

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

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

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

175 gnificant structure conservation between the PRV and HSV capsids.

176 ng and anterograde spread, we identified the PRV US9/gE/gI protein complex as a viral factor facilita

177 work for elucidating the early events of the PRV replicative cycle.

178 dissemination and relative virulence of the PRV strains.

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

180 We propose that the PRV anterograde sorting complex, gE/gI/US9, recruits KIF

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

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

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

184 irectly to virus injection sites, similar to PRV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 elled (prior injection of pseudorabies virus PRV-152) and whole-cell, patch clamp recordings were obt

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

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

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

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

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

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

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

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

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

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

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

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

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

219 plex virus 1 (HSV-1) and pseudorabies virus (PRV) in the infected cell cytoplasm is thought to involv

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

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

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

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

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

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

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

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

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

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

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

231 IF1A in axons.IMPORTANCE Pseudorabies virus (PRV) is an alphaherpesvirus related to human pathogens h

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

233 The alphaherpesvirus pseudorabies virus (PRV) is the causative agent of pseudorabies, a disease o

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

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

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

237 ed the structures of (i) Pseudorabies virus (PRV) RNA G-quadruplex and ligand complex, (ii) PRV DNA G

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

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

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

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

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

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

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

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

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

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

248 porcine alphaherpesvirus pseudorabies virus (PRV) was inhibited by sphingomyelin-depletion of cells.

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

250 sing isogenic strains of pseudorabies virus (PRV) with distinct fluorescent reporters (either eGFP or

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

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

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

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

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

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

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

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

259 herpesviruses, including pseudorabies virus (PRV), are neuroinvasive pathogens that establish lifelon

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

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

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

263 a-zoster virus (VZV) and pseudorabies virus (PRV), may cause cranial nerve disorder and unbearable pa

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

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

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

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

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

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

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

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

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

273 tracing with fluorescent pseudorabies virus (PRV).

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

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

276 nd attenuated strains of pseudorabies virus (PRV).

277 g recombinant strains of pseudorabies virus (PRV).

278 implex virus 1 (HSV1) or pseudorabies virus (PRV).

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

280 lly labeled by injecting pseudorabies virus (PRV-614) into the kidney, indicating reconnected seroton

281 ther alphaherpesviruses (pseudorabies virus [PRV] and herpes simplex virus 1 [HSV-1]).

282 Neither PR fraction (PRF) nor PR volume (PRV) correlated with RV end-diastolic volume (r = 0.36;

283 Supportive data from other VZV, PRV, and HSV1 laboratories about evidence for two egress

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

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 We investigated whether PRV used this entry pathway in multiple laboratory model

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

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

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

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

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

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

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

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

296 n and least utilized in HSV1 infection, with PRV's usage being closer to HSV1's usage.

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

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.