ライフサイエンスコーパス: virion

1 one RNA dimer is packaged into each nascent virion.

2 r, with 12 pentamers comprising a single HCV virion.

3 e expression of Vpr in trans in the incoming virion.

4 and to be efficiently packaged in the vector virion.

5 -energy structures available to the expanded virion.

6 ically aberrant multi-layered capsids in the virion.

7 ein dimer sequestered in the interior of the virion.

8 embrane, and it is not incorporated into the virion.

9 ocated on different capsid subunits from one virion.

10 the conversion temperature of wild-type (wt) virions.

11 al difficulty of separating VLVs from mature virions.

12 ilitating lateral spread of de novo-produced virions.

13 ng cells resulted in less infectious progeny virions.

14 e plasma membrane for packaging into progeny virions.

15 eate viral vesicles that continue to produce virions.

16 on of Vif to regulate infectivity of progeny virions.

17 ole in the entry and assembly of filamentous virions.

18 to efficiently isolate VLVs that are free of virions.

19 genomic DNA) versus empty (genome-free) HBV virions.

20 urrent paradigm confusing viruses with small virions.

21 protein-1, producing immature, noninfectious virions.

22 g profiles of NP for two H1N1 IAV strains in virions.

23 ponents come together to generate infectious virions.

24 of the viral core to form spherical immature virions.

25 ng largely spherical rather than filamentous virions.

26 defective particles and a decrease in intact virions.

27 e a major problem for the release of progeny virions.

28 ued HIV-1 infectivity, and was packaged into virions.

29 and packaging of unspliced genomic RNA into virions.

30 HA-tag on the surface of infected cells and virions.

31 predicted viral protease activity in single virions.

32 is a component of the tegument layer of VZV virions.

33 their subsequent enclosure to form immature virions.

34 the defects in axonal transport of enveloped virions.

35 ure due to a reduction in assembly of mature virions.

36 d for the efficient production of infectious virions.

37 eading to the efficient production of mature virions.

38 e essential host factors packaged into HIV-1 virions.

39 d subsequent extensive production of progeny virions.

40 d by p62 proteins, some of which lay between virions.

41 psid protein and is unable to produce mature virions.

42 this peptide physically destroyed influenza virions.

43 between the nucleocapsid and the envelope of virions.

44 ajor membrane protein of immature and mature virions.

45 the severe loss of production of infectious virions.

46 d for the efficient production of infectious virions.

47 formation and its enclosure to form immature virions.

48 cells correlated well with those on progeny virions.

49 ansport of unenveloped capsids and enveloped virions.

50 teins Gag and Gag-Pol, resulting in immature virions.

51 is virus and allow the production of progeny virions.

52 DNA and the downstream production of progeny virions.

53 ocalization despite failing to form immature virions.

54 plete virions, it is phosphorylated in empty virions.

55 the plasma membrane and is unable to entrap virions, activated NF-kappaB in concert with the Ebola v

56 nsmembrane proton channel that acidifies the virion after endocytosis.

57 agement of the infected cells not to produce virions after the "kick" step is important to this strat

58 l role in the envelopment of the cytoplasmic virion and its egress.

59 itical for the association of gp120 with the virion and that amino acid substitution increased the am

60 activity through clearance of IgG-opsonized virions and elimination of HIV-infected cells.

61 r understanding how humoral responses target virions and for developing related antiviral countermeas

62 Free virions and infected cells were not readily detectable b

63 nly HIV protein expressed on the surfaces of virions and infected cells.

64 ral protein expressed on the surface of both virions and infected cells.

65 essential step to generate infectious HIV-1 virions and is mediated by interactions between the vira

66 cific antibody inhibited hemagglutination by virions and ISVPs, probably via direct interference with

67 ted hemagglutination inhibition assays using virions and ISVPs.

68 and is antagonized by Nef and analyzed both virions and producer cells with quantitative lipid MS.

69 rfect colocalization of these two markers in virions and their fixed 1:1 ratio enabled automated dete

70 pants' sera were found to avidly capture HIV virions and to mediate antibody-dependent cellular phago

71 of tumor-associated gammaherpesviruses, both virions and VLVs are produced and are released into the

72 The TF protein is a component of budded virions, and optimal levels of TF correlate positively w

73 velope interaction to secrete DNA-containing virions, and the CTD state of phosphorylation also does

74 ells, providing instructions to generate new virions, and therefore is essential for virion infectivi

75 al replication centers, and the newly formed virions are able to infect HeLa cells.

76 HCV virions are believed to latch onto or fuse with the nasc

77 ucible mutant demonstrated that I2-deficient virions are defective in cell entry.

78 resence of FAS inhibitors, the intracellular virions are noninfectious, indicating that FAS is requir

79 viral RNA genome and IN from ALLINI-treated virions are prematurely degraded in target cells, wherea

80 BV tropism is dictated by gp42 levels in the virion, as it inhibits entry into epithelial cells while

81 C maturation and secretion of DNA-containing virions, as in DHBV.

82 matrix protein is the main driving force for virion assembly and budding.

83 with the structural protein Gag facilitates virion assembly and particle production.

84 2 in the restriction of HIV-1, also prevents virion assembly in a BST2-independent manner.

85 ectious, indicating that FAS is required for virion assembly or maturation.

86 t of 10 Giles proteins, including a putative virion assembly protein (gp17), the phage integrase (gp2

87 ly packaged because binding to Psi nucleates virion assembly with particular efficiency.

88 hepatocytes, participate in and regulate HBV virion assembly, capsid uncoating, and covalently closed

89 ed important insights into genome packaging, virion assembly, cell entry, and other stages of the vir

90 tions are the nucleation event of infectious virion assembly, ensuring that one RNA dimer is packaged

91 ular assembly platforms serving replication, virion assembly, or virus egress via budding out of infe

92 igh efficiency despite being dispensable for virion assembly.

93 nterrogations of respiratory syncytial virus virion assembly.

94 packaging signals playing essential roles in virion assembly.

95 g approximately 60 specific interactions for virion assembly.

96 h cognate viral proteins may be critical for virion assembly.IMPORTANCE Poxviruses are unique among e

97 delivery into the cytoplasm, but not in any virion-assigned step, such as cell binding, endosomal tr

98 ytomegalovirus (CMV) DNA exists in plasma as virion-associated or free DNA is uncertain.

99 tein trimers that mimic the structure of the virion-associated spike, which is the target for neutral

100 Native-like trimers mimicking virion-associated spikes present nearly all bnAb epitope

101 Viral transcription could be rescued by virion-associated Vpr.

102 to study a heterogeneous population of SBPV virions at pH 5.5.

103 ,2) antagonizes the trapping of newly formed virions at the plasma membrane by BST2, we found that it

104 fections: it traps newly assembled enveloped virions at the plasma membrane in infected cells, and it

105 ISAV entry requires the interplay of the virion-attached hemagglutinin-esterase and fusion glycop

106 Virion attachment to host cells is mediated by 20-nm-lon

107 dence that virus-Sia interactions may aid in virion attachment.

108 Poxvirus virion biogenesis is a complex, multistep process, start

109 cytoplasm to the plasma membrane leading to virion budding.

110 s the lysosomal degradation of trapped HIV-1 virions but also functions as a BST2-independent anti-HI

111 ted in decreased production of extracellular virions but did not reduce intracellular genome levels o

112 A gE-null mutant produced enveloped virions, but these accumulated in large numbers in the n

113 ly inhibited production of infectious budded virions (BV).

114 leading to induced production of infectious virions by targeted modulation of Gag PM targeting.

115 tron microscopy (cryo-EM) reconstructions of virion capsids did not detect any obvious differences in

116 ent cellular cytotoxicity, phagocytosis, and virion capture).

117 Each HIV-1 virion carries 10-14 Envs, and therefore a defective Env

118 We found that the majority of HIV-1 virions carry either only trimeric ("functional") or onl

119 Virion-cell and cell-cell fusion experiments revealed th

120 Low levels of virion CMV DNA were found in 10 of 103 (9.7%) samples wi

121 ncrease both in the cell and in the released virion compared to the wild type.

122 t of diverse host proteins that became major virion components.

123 es, and encode translation components; their virions contain >100 proteins as well as mRNAs.

124 Iflaviruses have nonenveloped icosahedral virions containing single-stranded RNA genomes.

125 e rate of viral production is rapid (>25,000 virions d(-1)), and the lifetime of an infected cell whi

126 Use of fluorescent HSV-1 virions demonstrated a pattern of viral spread ex vivo t

127 amics are also predicted, with simulation of virion-derived peptides suggesting that efficient proces

128 ssion that is resistant to tetherin but that virion dissemination via plasma is inhibited by tetherin

129 marker epitopes are dispersed to regions of virions distal to CD4 contact.

130 veloped to differentiate free naked DNA from virion DNA.

131 than reaching cell surfaces as wild-type HSV virions do.

132 lucidate the roles of tetherin and cell-free virions during in vivo viral dissemination and pathogene

133 s identified disparate effects on infectious virion egress from infected cells.

134 lternatively, it is possible that on a given virion either all the spikes are defective or all are fu

135 On virions, electron microscopy (EM) and tomography reveal

136 ototype BST2 antagonist, which inhibits both virion entrapment and the induction of NF-kappaB activit

137 lex gB/gH-gL mediates membrane fusion during virion entry and cell-cell fusion.

138 ceptor, triggering gB-mediated fusion of the virion envelope with cellular membranes.

139 The observation that the majority of virions exclusively express either functional or nonfunc

140 immediately after viral entry, with incoming virions failing to form replication complexes.

141 ggest that the A3G molecules packaged in the virion first deaminate viral DNA as monomers before dime

142 kaging of antirestriction components into P1 virions follows a distinct pathway that begins with the

143 is was interrupted at a stage after immature virion formation, resulting in the accumulation of dense

144 d for crescent formation, it is required for virion formation, suggesting that interactions of the N

145 array of hairpin structures plays a role in virion formation.

146 equired for AAV2 DNA replication and progeny virion formation.

147 Analysis of HIV-1 virions from participants infected in a randomized contr

148 which sorafenib inhibits the release of RVFV virions from the cell.

149 f HSV is irreversible and due to a defect in virion fusion activity.

150 We report single-virion fusion experiments, using methods developed in pr

151 Tight packing of the major virion glycoprotein (VP1) is ensured by extended hydroph

152 ses, 27 antibodies targeting epitopes in CMV virion glycoprotein complexes, including glycoprotein B

153 Glycoprotein K (gK) is a conserved virion glycoprotein of all alphaherpesviruses that is no

154 Newly formed virions have the capacity to infect other cells (HeLa).

155 infection of HEK293 and HeLa cells with AAV2 virions, HBoV1 NS2 (but not NS4), NP1, and BocaSR were r

156 n the generation of infectious extracellular virions (HSV(des)) that lack cholesterol and likely cont

157 In contrast, the CTD in empty HBV virions (i.e., enveloped capsids with no RNA or DNA) was

158 er of envelope glycoprotein (Env) spikes per virion, i.e., approximately 7 to 14.

159 ins and membrane-mediated release of progeny virions.IMPORTANCE IBDV is the most extensively studied

160 sids and the envelope for secretion of empty virions.IMPORTANCE The phosphorylation state of the C-te

161 in an acidic environment and release progeny virions in a membrane-mediated cell-to-cell manner.

162 the viral DNA and the production of progeny virions in HEK293 cells.

163 The capsids of SBPV virions in low pH are not expanded.

164 Rico/8/34 (H1N1) and A/Scotland/20/74 (H3N2) virions in MDCK cells.

165 ription in leukemia blasts as well as intact virions in serum.

166 , we show that incorporation of SERINC5 into virions in the absence of Nef inhibits the formation of

167 is critical for the production of infectious virions in various cell types and is sufficient for BAF

168 Malfunctioning of this machinery renders virions incapable of infecting cells.

169 arently exapted HERV-T env could not support virion infection but could block ancHTenv mediated infec

170 The virion infectivity factor (Vif) open reading frame is co

171 protein shell assembly is a prerequisite for virion infectivity in many multi-shelled dsRNA viruses.

172 new virions, and therefore is essential for virion infectivity.

173 ntributions to envelope protein function and virion infectivity.

174 Their ability to bind RNA is essential for virion infiltration and antiviral activity, yet the mech

175 monovalent inactivated AS03-adjuvanted split virion influenza A(H1N1)pdm09 vaccine (Pandemrix; GlaxoS

176 The egress of the genome from SBPV virions is associated with a loss of interpentamer conta

177 pairs, while the mean bottleneck size of 196 virions is consistent with a previous estimate for this

178 noninfectious HIV-1 particles to infectious virions is dependent upon the sequential cleavage of the

179 BCA2 prevent assembly and release of nascent virions, it also significantly restricts HIV-1 transcrip

180 Whereas CTD is unphosphorylated in complete virions, it is phosphorylated in empty virions.

181 ects on cell metabolism and/or on the vector virion itself.

182 Virions lacking the M25 tegument protein were of smaller

183 amics, and cellular location of uncoating of virions leading to infection has been confounded by defe

184 smic or viral environments or following cell/virion lysis and removal of proteins.

185 assembly of the conical viral capsid during virion maturation and results in perturbations at a spec

186 Is potently inhibit HIV-1 replication during virion maturation by inducing hyper- or aberrant IN mult

187 non-infectious, since other Env on the same virion may still be functional.

188 6 functions early during infection, enabling virion-mediated genome delivery into the cytoplasm, but

189 Vis-a-vis virion morphogenesis, an improper protein-protein intera

190 We concluded that I2 is required for virion morphogenesis, release of the D13 scaffold, and t

191 Thus, to establish a productive infection, virions must be stable in the environment but flexible t

192 VPS52 and VPS54 were dispensable for mature virion (MV) production but were required for extracellul

193 protein, and a symmetric ring in the mature virion (MV-portal) that has negligible affinity for the

194 roteins necessary for the budding of progeny virions needs to accumulate at budozones.

195 er transduction and provides protection from virion neutralization in mice.

196 fective Env may not necessarily render a HIV virion non-infectious, since other Env on the same virio

197 efficient entry and nuclear egress of budded virions of AcMNPV.IMPORTANCE Little is known regarding t

198 Virions of these viruses are composed of many different

199 d Huh7 cells, they can be infected by intact virions of transgenic hepatitis B.

200 er that correlated between cells and cognate virions (P = 0.027).

201 We find that virion-packaged Vpx proteins from a second SIV lineage,

202 ng but not the Vpx-SAMHD1 interaction or Vpx virion packaging.

203 tended time-lapse imaging with less than one virion per cell allows identification of infected cells

204 We also estimate that the minimum number of virions produced by an infected cell over its lifetime i

205 the producer cell and the infectivity of the virions produced.

206 , retains it in lipid rafts and blocks HIV-1 virion production and spread.

207 al genome increase LT levels and promote MCV virion production and transmission, which can be neutral

208 As, and host determinants in order to ensure virion production at the right place and right time.

209 inc-finger antiviral protein (ZAP) inhibited virion production by cells infected with CG-enriched HIV

210 Infectious virion production is activated by the essential viral Re

211 03) that are important for infectious budded virion production were found to associate with NSF, and

212 ng, viral RNA nuclear export, and infectious virion production.

213 cycle, contributing to efficient infectious virion production.

214 ing peak stages of lytic gene expression and virion production.

215 ellular genome levels or block intracellular virion production.

216 e latently infected cells without increasing virion production.

217 The HSV-1 virion protein 13/14 (VP13/14), also known as UL47, is a

218 ive sequence and structure analysis of major virion proteins indicates that they evolved on about 20

219 ral structures in the absence of other major virion proteins.

220 the activation of influenza A/Scotland/20/74 virions, providing further evidence of its importance.

221 al replication was determined by RT-qPCR and virion release by TCID50 assay.

222 or low intracellular protein expression and virion release.

223 viral DNA synthesis, nuclear migration, and virion release.

224 or viral entry, intracellular migration, and virion release.

225 ET of spleen revealed thousands of virions released by individual cells and discreet cytopl

226 Using a PV replicon and purified virion RNA, we also show that eIF4E promotes the rate of

227 The role of CTD phosphorylation in virion secretion, if any, has remained unclear.

228 le of the state of phosphorylation of CTD in virion secretion, we have analyzed the CTD phosphorylati

229 TD state of phosphorylation may not regulate virion secretion.

230 r with efficient pre-F packaging into vector virions, significantly increased F immunogenicity in the

231 r regulation of gene expression, or enhanced virion stability and cell-to-cell movement.

232 CD-loop in cell-type-dependent replication, virion stability, and in vivo pathogenesis.

233 Both the virion structural properties and the genome content supp

234 ling the similarities and the differences in virion structure and function between ZIKV and related f

235 and putative catalytic sites within the DWV virion structure enables future analyses of how DWV and

236 Here, we present the virion structures of DWV determined to a resolution of 3

237 here is a paucity of information on archaeal virion structures, genome packaging, and determinants of

238 , replication and expression strategies, and virion structures.

239 ical process in the production of infectious virions subsequent to DNA replication.

240 Proteomic analysis of purified virions suggests that packaging of antirestriction compo

241 e the only virally expressed proteins on the virion surface and are required for receptor binding.

242 lutinin (HA), a glycoprotein abundant on the virion surface, is important in both influenza A virus a

243 e/Membrane proteins, which together form the virion surface.

244 e via dynamic 'breathing' of E dimers at the virion surface.

245 obular protruding (P) domain, exposed on the virion surface.

246 form to mimic the native Env present on the virion surface.

247 essential processes, assembly of infectious virions, takes places in the cytoplasmic viral assembly

248 (SIVsmm/SIVmac/HIV-2) lineage packaged into virions target SAMHD1 for proteasomal degradation, incre

249 s viral DNA replication and produces progeny virions that are infectious in HAE.

250 ates the critical balance between assembling virions that are stable and maintaining conformational f

251 The relatively small subfraction of virions that carry both functional and nonfunctional Env

252 ng the immature procapsid, the genome-filled virion, the putative entry intermediate (A-particle), an

253 are exposed across the surface of cell-bound virions, thus explaining their immunoreactivity.

254 pesviruses enter cells via attachment of the virion to the cellular surface and fusion of the viral e

255 icroscopy demonstrated that sorafenib caused virions to be present inside large vacuoles inside the c

256 change during the proteolytic disassembly of virions to infectious subvirion particles (ISVPs) that a

257 Preexposure of isolated virions to mildly acidic pH of 5 to 6 partially inactiva

258 This suggests that exposure of virions to the cell culture medium is obligatory during

259 a structural rearrangement of sigma1 during virion-to-ISVP conversion and contribute new information

260 Virion transmembrane proteins (VTPs) mediate key functio

261 research on alloherpesvirus VTPs.IMPORTANCE Virion transmembrane proteins play key roles in the biol

262 for the further research on alloherpesvirus virion transmembrane proteins.

263 findings were: (i) the FL strain encodes 16 virion transmembrane proteins; (ii) eight of these prote

264 This characterization of the virion transmembrane proteome of CyHV-3 provides a firm

265 In this study of the virion transmembrane proteome of CyHV-3, the major findi

266 ation, the nonenveloped human papillomavirus virion uncoats in the endosome, whereupon conformational

267 as genomic RNAs (gRNAs) packaged by Gag into virions undergoing assembly at the plasma membrane (PM).

268 investigate Env conformations on individual virions using our new nanotechnology, "flow virometry",

269 y reduced viral replication, indicating that virions utilized the low-pH environment of acidic organe

270 By stabilizing unique structures of expanded virions, VHH binding permitted a more detailed view of t

271 Here, we determined structures of Qbeta virions, virus-like particles, and the Qbeta-MurA comple

272 The intracellular accumulation of RVFV virions was also observed in cells transfected with siRN

273 the biogenesis of quasi-enveloped HAV (eHAV) virions, we conducted a quantitative proteomics analysis

274 plication but avoid production of infectious virions, we developed "single-cycle" adenovirus (SC-Ad)

275 ate of infectious-RNA incorporation into new virions, we developed a new recombinant reovirus S1 gene

276 Remarkably, incoming virions were able to supply sufficient ORF52 to induce M

277 observed that a large number of intact IBDV virions were arranged in a lattice surrounded by p62 pro

278 When HIV virions were generated in cells overexpressing polypepti

279 the viral genome, and the release of mature virions were impacted by the reduction of cellular chole

280 1-infected cells surrounded by pools of free virions were present in 10% of intestinal crypts by 10-

281 ltiple iterations of FACS, cells and progeny virions were shown to display higher levels of antigenic

282 In cells expressing DN NSF, entering virions were trapped in the cytoplasm or transported to

283 etained the D13 scaffold protein of immature virions, were severely deficient in the transmembrane pr

284 onformation close to that of Env spikes on a virion, whereas its monomeric gp120 exposes many nonneut

285 For secretion of empty HBV virions, which is independent of either viral RNA packag

286 Using SIV virions whose spikes were "decorated" with the primary c

287 Additionally, by comparing the Qbeta virion with Qbeta virus-like particles that lack a matur

288 also produce abnormally high proportions of virions with aberrant small heads, which suggests Hdf an

289 without a loss in infectivity and results in virions with abnormal morphology.IMPORTANCE Most of the

290 on microscopy analyses showed association of virions with developing sperm within testes as well as w

291 that HIV-1 RNA is selectively packaged into virions with high efficiency despite being dispensable f

292 the exact site where the association of HCV virions with host lipoproteins occurs.

293 Three-hour treatment of HSV-1 virions with pH 5 or multiple sequential treatments at p

294 The first block is during viral entry, where virions with relatively acid-stable hemagglutinin (HA) p

295 cal particles instead of brick-shaped mature virions with well-defined core structures.

296 mber of encapsidated aptamer transcripts per virion, with saturation occurring around 1:1 stoichiomet

297 n severely impaired production of infectious virions, with a decrease as great as 5 logs.

298 e in virus infection and caused a buildup of virions within cells.

299 secretory pathway, resulting in a buildup of virions within dilated ER vesicles.IMPORTANCE In humans,

300 Conversely, cell-free MLV and VSV virion yields and VSV spread to distal cells were dramat