ライフサイエンスコーパス: virion

1 ing multiscale simulations of the SARS-CoV-2 virion.

2 translation and as a genome for the progeny virion.

3 h can extend hundreds of nanometers from the virion.

4 on and immune evasion but is absent from the virion.

5 l as of the DNA-containing capsid inside the virion.

6 coarse-grained (CG) model of the SARS-CoV-2 virion.

7 ssembling more functional S protein into the virion.

8 and higher S-protein incorporation into the virion.

9 ex that is central to building an infectious virion.

10 or surface of the membrane of the assembling virion.

11 ach Fab can simultaneously occupy the mature virion.

12 protective epitopes but only bind the mature virion.

13 cruitment to VIs and before incorporation of virions.

14 til it eventually reactivates to produce new virions.

15 st to undergo autolysis and liberate progeny virions.

16 neck size in some cases, of between 1 and 13 virions.

17 enting the incorporation of A3G into progeny virions.

18 ma membrane, where it also binds to RSV-F on virions.

19 atalyze membrane fission and to free progeny virions.

20 infection by both naked and quasi-enveloped virions.

21 1 infectivity when incorporated into budding virions.

22 cted cells are also infectious and transport virions.

23 RINC5, inhibit the infectivity of retroviral virions.

24 f the genome is icosahedrally ordered within virions.

25 tracellular mature virions and extracellular virions.

26 was genetically identical to plasma-derived virions.

27 ning the proper tegument composition of HCMV virions.

28 ariants, co-assembling with L2 to infectious virions.

29 heir translation and the assembly of progeny virions.

30 irus bud from the host membrane as enveloped virions.

31 viral RNA replication and packaging into new virions.

32 ns and thereby prevents their packaging into virions.

33 nfection of primary keratinocytes with HPV16 virions.

34 ndings from an assessment of CA stability in virions.

35 favouring the formation of functional T = 3 virions.

36 rtant for the release of infectious poxvirus virions.

37 increasing the infectivity and stability of virions.

38 t fails to produce late genes and infectious virions.

39 he surface organization of these pleomorphic virions.

40 into the envelope of released extracellular virions.

41 sorting and transport of newly assembled PRV virions.

42 stributed among three physically homogeneous virions.

43 her properties of viral surface antigens and virions.

44 t necessarily indicate shedding of infective virions.

45 riant grows to a higher titer as pseudotyped virions.

46 to all three viral particle forms-the mature virion, A-particle, and empty particle-and show that eac

47 Surprisingly, electron microscopy revealed virions accumulated within the nucleus of amoebae.

48 st samples containing inactivated SARS-CoV-2 virions, added to in vitro derived mucus.

49 show that MAL is involved in trafficking of virions along cell processes and that MAL depletion prod

50 The capsid is an essential component of the virion and it is therefore of interest how it assembles

51 nctions: compaction of the RNA genome in the virion and regulation of viral gene transcription.

52 ted infectious microvesicles containing both virions and a unique morphological component that we des

53 py and tomography to image intact SARS-CoV-2 virions and determine the high-resolution structure, con

54 nveloped virions termed intracellular mature virions and extracellular virions (EV).

55 nveloped virions termed intracellular mature virions and extracellular virions.

56 NAs that encode the structural components of virions and include viral genomic RNAs.

57 essing the M2 channel, as well as, influenza virions and MDCK-ATL cells infected with influenza virus

58 inase (CD) APOBEC, binds RNA to package into virions and restrict HIV-1 through deamination-dependent

59 itor) that has a matched nanotopology to IAV virions and shows heteromultivalent inhibitory effects o

60 ing cells reduces the infectivity of progeny virions and that HIV-1 infection reduces the cell surfac

61 hat CVA16 vaccines should be based on mature virions and that these antibodies could be used to discr

62 ed in two distinct populations - one as free virions and the other enclosed within membranes.

63 ity by altering the conformation of gp120 on virions and/or physical masking of specific HIV-1 Env ep

64 results reveal the conformations of S on the virion, and provide a basis from which to understand int

65 own that its genome is highly ordered within virions, and that it regulates the assembly process of t

66 tures of Env trimer embedded in AT-2-treated virions appear well-represented by current engineered tr

67 called viral inclusions (VIs) where progeny virions are assembled.

68 ulating evidence suggests that, in solution, virions are highly dynamic assemblies.

69 These quasi-enveloped virions are infectious and are the only form of virus th

70 Poliovirus virions are nonenveloped icosahedral 30-nm particles wit

71 uptake into the endocytic compartment, where virions are proteolytically converted to infectious subv

72 Extracellular virions are required for cell-to-cell spread and pathoge

73 By contrast, non-enveloped naked virions are shed in faeces and stripped of membranes by

74 reactivations, during which newly assembled virions are sorted into and transported anterogradely in

75 trengths ranging from < 0.01 to 0.02 M, rNDV virions are spherical or predominantly spherical.

76 piratory syndrome coronavirus 2 (SARS-CoV-2) virions are surrounded by a lipid bilayer from which spi

77 membrane-fusion points, through which mature virions are transported.

78 surface and increased Env incorporation into virions as the determinants for the Nef- and CD3-depende

79 nactivation protocol capable of inactivating virions, as well as endogenous nucleases, was optimized

80 ses following trypsin digestion of the three virions assembled separately in vivo using the Agrobacte

81 nd utilization of host exosome machinery for virion assembly and egress.

82 replication, transcription, translation, and virion assembly occur at sites within the cytoplasm know

83 A synthesis, transcription, translation, and virion assembly occur.

84 amine lambda DNA replication, transcription, virion assembly, and resource recruitment in single-cell

85 Both proteins enhance virion assembly, but C16/B22 increases proteolytic proce

86 f viral polymorphism and study mechanisms of virion assembly.

87 s and thereby coordinate ESCRT function with virion assembly.

88 Virion-associated MAPK/ERK-2-mediated phosphorylation of

89 with virion morphology and Mn(2+)-dependent virion-associated reverse transcriptase activity typical

90 We have used fusion inhibitors to trap HIV-1 virions attached to target cells by Envs in an extended

91 These proteins also inhibited virion attachment to CD4(-) lymphoid organ fibroblastic

92 s developed techniques for identification of virions based on a modular atomic force microscopy (AFM)

93 bodies could be used to discriminate optimal virion-based immunogens.

94 Using a unique ZIKV virion-based sorting strategy, we isolated and character

95 as been difficult to identify the infectious virions because only one of ~50 virions in infected cell

96 ural similarity to those found in infectious virions before cell entry were observed upon mutation of

97 eBD1, -2, and -3 resulted in increased EHV1 virion binding to and infection of these cells.

98 In addition, virion binding to and subsequent infection of respirator

99 Electron tomography revealed HIV-1 virions bound to TZM-bl cells by 2-4 narrow spokes, with

100 sion assay, we observed that while fusion of virions bound to vesicles coated with sialylated mucin m

101 assembles at the plasma membrane and drives virion budding, assisted by the cellular endosomal compl

102 , and atazanavir, which reduces the cellular virion burst size and hence inhibits replication only af

103 nhanced exclusion of the mutant protein from virions by Nef.

104 substitutions compromised IN-RNA binding in virions by one of the three distinct mechanisms: (i) mar

105 ng of CA with GFP and to identify infectious virions by tracking viral cores in living infected cells

106 We demonstrate that virions can reliably infect and lysogenize hosts by hija

107 L1 and L2 capsid proteins self-assemble into virions capable of efficiently packaging either its 8 ki

108 e dose of AcrVIA1 delivered by an individual virion completely dismantles type VI-A CRISPR-mediated i

109 t the cryo-EM structure of the complete ASFV virion, comprising a viral particle of multiple layers,

110 t of the PtdIns(3)P-binding protein WIPI2 to virion-containing endosomes.

111 These virion-containing MCs emerged from larger, LAMP-1-positi

112 d RNA2, respectively, while type 3 (B3+4(V)) virions copackage genomic RNA3 (B3) and its subgenomic R

113 Electron micrographs of infectious virions depict particle-associated CP-delta fibers with

114 ell by rapidly and directly interacting with virions, destabilizing the viral envelope, and driving v

115 e neuronal cytoplasm, which explains why HSV virions do not enter axons.

116 al membrane compared to intracellular mature virions due to a wrapping process at the trans-Golgi net

117 argo was subsequently incorporated into HCMV virions during infection.

118 Estimates of airborne virion emission rates while speaking strongly support th

119 icornaviruses in general, transport multiple virions en bloc via infectious extracellular vesicles, 1

120 After virions enter the host cell, they replicate to produce m

121 Our experiments suggest that GA inhibits virion entry by blocking the initial fusion event.

122 It is situated on the virion envelope and plays key roles in LASV growth, cell

123 r protection against HCMV infection, and the virion envelope glycoprotein B (gB) serves as a major ta

124 lla-zoster virus (VZV), induce fusion of the virion envelope with cell membranes during entry, and be

125 st regulators involved in viral trafficking, virion envelopment, and release.

126 rus and glycans, which provides insight into virion environmental stability and transmission.

127 tracellular mature virions and extracellular virions (EV).

128 In the first case, virions exit into the extracellular space and then infec

129 al M1 oligomers similar to those observed in virions exposed to the low pH of cell entry.

130 tein to direct incorporation into the vector virion for increased immunogenicity.

131 Isolating virions for determining high-resolution structures has b

132 l transcription/replication, and two inhibit virion formation and budding.

133 xviruses and have roles during extracellular virion formation and subsequent infection.

134 y affect virion morphology or the release of virions from cells.

135 After binding, virion gD interacts with a receptor to activate the regu

136 resulting in the loss of multiple lytic and virion genes.

137 ngth HIV-1 RNA from a large pool of mRNAs as virion genome during virus assembly.

138 human HSV vaccine is an understanding of the virion glycoproteins involved in entry.

139 Immature human immunodeficiency virus (HIV) virions have a lattice of Gag and Gag-Pol proteins ancho

140 pounds against HCMV via direct engagement of virions.IMPORTANCE Human cytomegalovirus (HCMV) is major

141 restriction by preventing its packaging into virions.IMPORTANCE MLV has existed in mice for at least

142 NA enzymatic stability and the NA amount in virions.IMPORTANCE N-linked glycans are transferred to s

143 o-electron microscopy structures of the EV71 virion in complex with Fab fragments of these potent and

144 r promoting the sorting and transport of PRV virions in axons.

145 t TFEB activation facilitates the release of virions in extracellular vesicles via secretory autophag

146 RL13 impaired, and produces low infectivity virions in fibroblasts, whereas TB40/e (TB) and TR are l

147 e infectious virions because only one of ~50 virions in infected cells leads to productive infection.

148 eneous population of spherical and elongated virions in isotonic (physiologic salt concentration) and

149 v trimers on aldrithiol-2 (AT-2)-inactivated virions in ligand-free, antibody-bound and CD4-bound for

150 followed by infection of the labeled mutant virions in mammalian cells in the presence of NAbs.

151 ispensable for production of infectious HCMV virions in multiple HCMV strains and cell types.

152 (eVP40) orchestrates assembly and budding of virions in part by hijacking select WW-domain-bearing ho

153 /ORF50 nor the production of infectious KSHV virions in PEL.

154 Correspondingly, I/LnJ CD300LF bound MNV virions in permissive cells but not in nonpermissive cel

155 using the GFP signal to guide imaging of HIV virions in primary co-culture.

156 aining confirmed enhanced replication of the virions in the absence of functional CD4(+) T cells in t

157 and were transported as capsids rather than virions in the axon.

158 on sites on the NA head domain contribute to virion incorporation and replication.

159 y ligand CD58 while promoting maturation and virion incorporation of glycoprotein O, a receptor bindi

160 In this study, we found that virion incorporation of PSGL-1 and CD43 closely correlat

161 In SERINC5-transfected 293T cells, virion incorporation of SERINC5 was increased by dimeriz

162 -1 infectivity and viral spread by enhancing virion incorporation of SERINC5.

163 viral proteins, both of which likely require virion incorporation of these proteins.

164 e SERINC5 and was associated with decreasing virion infectivity and viral replication in primary lymp

165 V-1 Nef plays an essential role in enhancing virion infectivity by antagonizing the host restriction

166 express a viral accessory protein called the virion infectivity factor (Vif), which recruits A3 prote

167 and CD43 closely correlates with diminished virion infectivity.

168 action pulls the Mat-gRNA complex out of the virion into the T4SS channel, causing a torsional stress

169 e up HSV-1 via endocytosis and transport the virions into multivesicular bodies (MVBs).

170 mbly of virus particles and sorting of these virions into neuronal axons.

171 rting enzyme 2 receptor and mediate entry of virions into target cells(2-6).

172 to the L2 capsid protein and sorts incoming virions into the retrograde transport pathway for traffi

173 d, by inference, oncolytic activity) of rNDV virions is fully maintained in their pleomorphic forms.I

174 The most abundant protein in influenza virions is matrix protein 1 (M1), which mediates virus a

175 Although the presence of gRNA in virions is required for viral infectivity, in its absenc

176 own that HIV-1 Vpr, a protein carried in the virion, is important for efficient infection of primary

177 w it oligomerizes to mediate the assembly of virions, is unknown.

178 gate interactions with glycans at the single-virion level directly on living mammalian cells, which o

179 , and study these interactions at the single-virion level.

180 cytomegalovirus (CMV) showed that virion-to-virion levels of pp71 tegument protein-the major viral t

181 on), as well as the rate at which infectious virions lose infectivity.

182 To expand the molecular knowledge governing virion maturation, we analysed HCMV virions using proteo

183 ial role of IN-RNA interactions for accurate virion maturation.

184 state, which is modeled to be on pathway for virion membrane fusion with target cells.

185 Specific to the extracellular virion membrane, glycoproteins A33, A34, and B5 are high

186 ry of enveloped viruses by binding PS in the virion membrane.

187 d incorporation into the outer extracellular virion membrane.

188 s, which were then assembled into a complete virion model.

189 d the gibbon ape leukemia virus (GALV), with virion morphology and Mn(2+)-dependent virion-associated

190 double mutation did not substantially affect virion morphology or the release of virions from cells.

191 es encoding protein components of the mature virion, namely, A26L, G6R, and A14.5L, achieved 74% to 9

192 electron microscopy images of just 2,048 EBV virions obtained by chemical induction.

193 tent in one of the three otherwise identical virions of a multipartite RNA virus, brome mosaic virus

194 able to probe structural organization of the virions of Herpes Simplex Type 1 viruses and bacteriopha

195 w in UL128-131, are RL13 intact, and produce virions of much higher infectivity.

196 Superresolution imaging of individual virions of the human herpesvirus cytomegalovirus (CMV) s

197 Ubiquitinated E is present on infectious virions of ZIKV when they are released from specific cel

198 2 and -3 also caused the aggregation of EHV1 virions on the cell surface of RK13 cells.

199 od representation of Env on the surface of a virion or an infected cell.

200 hese extracts directly inhibit extracellular virions or viral attachment to the human host cell as we

201 Some poxviruses sequester infectious virions outside of the factories in inclusion bodies com

202 s precluded understanding of how herpesvirus virions overcome the abundant mucosal beta-defensins dur

203 Type 1 (B1(V)) and type 2 (B2(V)) virions package genomic RNA1 and RNA2, respectively, whi

204 omes of all crAss-like phages encode a large virion-packaged protein(2,4) that contains a DFDxD seque

205 Virion-packaged Vpr is released in target cells shortly

206 ydrophobic interface of A3G does not abolish virion packaging and HIV-1 restriction.

207 ch only one RNA-binding mode is critical for virion packaging and restriction of HIV-1 by A3G.

208 multimerization is linked to RNA binding and virion packaging for HIV-1 restriction.

209 nhibited state, which probably occurs before virion packaging.

210 tein abundance within individual herpesvirus virion particles enables probabilistic bet hedging betwe

211 odically replicate and produce viable herpes virions, particularly in anogenital and cervical tissues

212 Released virions play a key role in latent reservoir maintenance

213 secreted microvesicles, including mature PV virions; positive-sense genomic and negative-sense repli

214 moted alternate replicative strategies: high virion pp71 levels enhance viral replicative fitness but

215 t, strikingly, impede silencing, whereas low virion pp71 levels reduce fitness but promote silencing.

216 Virions present in samples persisted over the experiment

217 Virions produced in the absence of UL88 exhibit decrease

218 f 15 late lytic genes that are important for virion production and infectivity is particularly depend

219 own (KD) impairs HCV replication and reduces virion production.

220 eins are produced, culminating in infectious virion production.

221 due to proliferation of infected cells with virion production.

222 ve factors for lytic cycle transcription and virion production.

223 dically expressed at low levels without full virion production.

224 their likeness to the matrix layer of intact virions prompted structural analysis by cryo-electron mi

225 .IMPORTANCE The vaccinia virus extracellular virion protein F13 is required for the production and re

226 the major capsid protein and other predicted virion proteins, including three RNA polymerase subunits

227 si-enveloped particles and apically as naked virions, recapitulating essential steps of the natural i

228 uman BST-2 expression, and facilitated HIV-1 virion release in the presence of human BST-2.

229 New hepatitis B virions released from infected hepatocytes are the resul

230 over the experimental time period, with most virions remaining infectious.

231 The release of infectious virions requires the production of capsid proteins and o

232 -bound capsid tetramers are assembled inside virions, resulting in defective uncoating of nucleocapsi

233 nteractions between incoming, pre-replicated virion RNA and host protein factors are important in inf

234 Mechanistically, m(6)A-deficient virion RNA induces higher expression of RIG-I, binds mor

235 ly occur between proteins and pre-replicated virion RNA.

236 their prevalences in cytoplasmic RNA and in virion RNA.

237 With VIR-CLASP, only the incoming virion RNAs are labeled with 4SU, so crosslinking events

238 ted in m(6)A-deficient recombinant HMPVs and virion RNAs that induced increased expression of type I

239 pparently, general principles fundamental to virion-sialoglycan interactions prompted convergent evol

240 nal space, with implications for maintaining virion stability and infectivity.

241 rface attachment factors and also may impact virion stability and virus replication.

242 AAVv66 exhibits enhanced production yields, virion stability, and CNS transduction.

243 mer, can bind poliovirus but fail to enhance virion stability.

244 s can bind to poliovirus but do not increase virion stability.

245 Virion stabilization required binding of long GlcNAc pol

246 ngth requirements, and thus the mechanism of virion stabilization, have been unclear.

247 50-200 genes, of which 15-35 are involved in virion structure and assembly, DNA packaging, lysis, and

248 phage validated the predicted podovirus-like virion structure and the identity of the major capsid pr

249 fragments of VI have been identified in the virion structure.

250 However, the specific infectivity of HCMV virions suffers in the absence of UL88, as more genomes

251 ifferent dynamics for the three types of BMV virions, suggest that the different RNA genes they conta

252 HIV-1 cores released from permeabilized virions supported efficient, capsid-dependent endogenous

253 t the structure and distribution of S on the virion surface remain unknown.

254 , with numerous filaments extending from the virion surface, expands our understanding of viral diver

255 and distribution of S trimers in situ on the virion surface.

256 ng the viral proteins UL47 and UL48 into the virion tegument layer.IMPORTANCE A better understanding

257 report that several epitopes from the HSV-1 virion tegument protein (VP11/12) encoded by UL46 are ta

258 This may be a result of altered virion tegument protein composition, as Western blot ana

259 antigenically distinct, infectious enveloped virions termed intracellular mature virions and extracel

260 antigenically distinct infectious enveloped virions termed intracellular mature virions and extracel

261 ibited entry via direct interaction with the virion that impeded binding to the plasma membrane.

262 re spokes present when evaluated with mutant virions that lacked the Env cytoplasmic tail.

263 , since antibodies to NS1 do not bind to the virion, thereby eliminating the risk of ADE.

264 M3 reduces membrane fusion between cells and virions through a poorly characterized mechanism.

265 ells, and intermittently produces infectious virions through lytic replication.

266 s, envelope glycoproteins bind the infecting virion to cell-surface receptors and mediate membrane fu

267 solved in complex with chimeric Sindbis/EEEV virions to 7.2 angstrom and 8.3 angstrom, respectively.

268 onal change in sigma1 from a compact form on virions to an extended form on ISVPs.

269 We studied the fusion of influenza virus virions to endosomes in a chemically controllable manner

270 ng HBV relaxed circular DNA delivered by the virions to hepatocytes.

271 They then lyse the host, releasing virions to infect new cells.

272 eled lipids to the viral membrane, we tether virions to lipid-labeled target vesicles and use fluores

273 e efficient wrapping of intracellular mature virions to produce EV and which plays a role in EV entry

274 erpesvirus cytomegalovirus (CMV) showed that virion-to-virion levels of pp71 tegument protein-the maj

275 Following attachment and internalization, virions traffic to late endosomes where GP is cleaved by

276 we show that herpes simplex virus 1 (HSV-1) virions travel in association with MAL-positive structur

277 xpression system allowed us to assemble each virion type separately in planta Experimental approaches

278 In the absence of gangliosides, both virion types are efficiently internalized through endocy

279 c mobility failed to distinguish between the virion types.

280 In addition, after secretion the virions undergo a distinct maturation step during which

281 overning virion maturation, we analysed HCMV virions using proteomics, and identified a significant p

282 the high-resolution structure of the mature virion, VI and VII may compete for the same binding site

283 transcription and the formation of complete virions via an interaction with the viral protein NP.

284 rimeric structures and are incorporated into virions via noncovalent interactions.

285 ith genome length varying a thousandfold and virion volume nearly a millionfold.

286 The purified virions were isometric with an estimated diameter of 33

287 viral RNA was detected within spores, mature virions were not observed.

288 n of regulatory factors, especially when the virions were opsonized with complement factors.

289 nst many bacterial and viral pathogens, EHV1 virions were resistant to eBDs through the action of the

290 Pretreatment of EHV1 virions with eBD2 and -3 increased the subsequent infect

291 in a striped-snakehead fish cell line, 35-nm virions with flaviviral morphology were visualized using

292 ted in the recovery of replication-competent virions with low susceptibility to the inhibitor.

293 orphologically indistinguishable icosahedral virions with T=3 quasisymmetry.

294 es the fusion of the lipid envelope of their virions with the host lipid membrane though a stepwise a

295 Our results show that the ASFV virion, with a radial diameter of ~2,080 angstrom, enclo

296 shell is 'collapsed' compared to the mature virions, with molecules pushed inwards at the icosahedra

297 ET) of the egress zones revealed clusters of virions within membrane-bound structures, which we term

298 ture ATI protein aggregation and trapping of virions within the factory.

299 lity to mediate immune exclusion by trapping virions within the glycocalyx and preventing the virus f

300 ypothesized that proliferating cells produce virions without HIV replication.