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1 rimer set for bacteriophage MS2 (a model RNA virus particle).
2 nformations in the context of the infectious virus particle.
3 ral protease into the proteins that form the virus particle.
4 in expressed in the cell and packaged in the virus particle.
5 m the known hexagonal protein lattice in the virus particle.
6 ssed only when E proteins are assembled on a virus particle.
7 opy of each RNA segment is packaged into one virus particle.
8 epitope located at the surface of the dengue virus particle.
9  budding, which then constitutes part of the virus particle.
10 s in virus assembly and in the morphology of virus particles.
11 mental force-deformation spectra for several virus particles.
12 ered to be packaged efficiently into vaccine virus particles.
13 otein crucial for the optimal infectivity of virus particles.
14 ein lattices that drive assembly of immature virus particles.
15 e cells to recognize genomes within incoming virus particles.
16  mediated by exosomes rather than infectious virus particles.
17 host factors to optimally produce infectious virus particles.
18 , but there was very little C3 deposition on virus particles.
19 ermine the position of protein layers within virus particles.
20 s cells to recognize genomes within incoming virus particles.
21 significantly higher IFN responses than free virus particles.
22 and the A17 membrane protein for assembly of virus particles.
23 s to budding and release of progeny immature virus particles.
24 erely attenuated upon depletion of GSLs from virus particles.
25 een the nucleocapsid and the envelope within virus particles.
26 stponed and reduced production of infectious virus particles.
27 tes the properties of ApoE on the surface of virus particles.
28 FN-gamma resulted in a reduced production of virus particles.
29 sates from both infected cells and disrupted virus particles.
30 binds lipids, and regulates formation of new virus particles.
31 h in the isolated recombinant protein and in virus particles.
32 s (uncoating) as well as assembly of progeny virus particles.
33 excluded hundreds of superinfecting vaccinia virus particles.
34 preparations of both Sindbis and Chikungunya virus particles.
35 ates assembly and egress of infectious Ebola virus particles.
36 form for detection and diagnostics of intact virus particles.
37 s structures resembling native Env spikes on virus particles.
38 bilization and the intracellular motility of virus particles.
39 ch reduced amounts of often markedly smaller virus particles.
40 brane formation and the assembly of immature virus particles.
41 tructural protein Gag or its accumulation in virus particles.
42 tely 1 to 2% of BM cells produced infectious virus particles.
43 tries, and dimensions that match the size of virus particles.
44 tential for exposure to VEEV via aerosolized virus particles.
45 this often remains incomplete for infectious virus particles.
46 nt of BBLF1 to achieve optimal production of virus particles.
47 pating in budding or being incorporated into virus particles.
48 ull-length Gag protein was incorporated into virus particles.
49 erful tool to visualize and track individual virus particles.
50  assemble trimer-clustered T = 3 icosahedral virus particles.
51  down to attomole levels and as few as 10(6) virus particles.
52 r reminiscent of the cell-surface docking of virus particles.
53 ressive assembly, and packaging into progeny virus particles.
54  PD that result in intercellular movement of virus particles.
55 strates for RNA synthesis and packaging into virus particles.
56 g to HA on the surface of infected cells and virus particles.
57 oduction, thereby increasing the chances for virus particle acquisition by aphid vectors and CaMV tra
58  is required for complete budding of Sindbis virus particles although several different amino acids c
59 s, termed HK2, still is capable of producing virus particles, although these particles have been rega
60 n of RT and, in some cases, integrase in the virus particle and this abolishes infectivity.
61 ed cell culture supernatant was enriched for virus particles and a generic, PCR-based method was used
62 n between the glycosphingolipid (GSL) GM3 on virus particles and CD169/Siglec-1 on MDCs.
63 rafficking pathways to effect the release of virus particles and disrupts the structure of the Golgi
64 ucture, dynamics, and biological function in virus particles and other large protein cages.
65           Like Nef, S2 excludes SERINC5 from virus particles and requires an ExxxLL motif predicted t
66 led that the vaccine contained visible split-virus particles and retained the native conformation of
67 y blocked post-entry long-range transport of virus particles and suppressed infection approximately 5
68  vesicular compartments or surface-localized virus particles and that large fluorescent signals corre
69 h a thin layer of a composite containing M13 virus particles and the electronically conductive polyme
70 onstrated to be by both the direct action on virus particles and the interference on the host cells.
71 otein (Env) spike, located on the outside of virus particles and the only relevant protein for the in
72 antitative analysis of fluorescently labeled virus particles and virus neutralization assays, we show
73 hat it is in a higher-order structure in the virus particle, and provide the first direct evidence th
74 lamentous and branched respiratory syncytial virus particles, and assembly with genomic ribonucleopro
75 d incorporates more VP26 fusion protein into virus particles, and individual virus particles exhibit
76 racellular infectivity, thermal stability of virus particles, and NS2 interactions.
77 observed to impair Env protein assembly into virus particles, and several of these are suppressed by
78  the incorporation of IAV gene segments into virus particles, and this process is thought to be media
79 e mechanisms by which infectious hepatitis C virus particles are assembled and released from the cell
80        Efficient replication and assembly of virus particles are integral to the establishment of inf
81 e studies demonstrate that noncapped Sindbis virus particles are produced as a result of viral RNA sy
82 to changes in environmental conditions after virus particles are released from the host cells.
83 e input virus, suggesting that a fraction of virus particles are resistant to antibody neutralization
84  anterograde axonal transport, ensuring that virus particles are transported from the cytoplasm into
85 e contrast using ice-embedded tobacco mosaic virus particles as test samples at 20-80 keV electron en
86 luorescence microscopy can detect individual virus particles as they enter cells, allowing us to map
87  proteins have important roles in assembling virus particles as well as modifying host cells to promo
88                     In all cases, the mutant virus particles, as well as the antibody-bound wild-type
89 ranules suggest that they may be sites where virus particles assemble.
90          However, the mechanisms involved in virus particle assembly and egress are still elusive.
91 ributions of MA-mediated membrane binding to virus particle assembly are not well understood.
92               Retroviral Gag proteins direct virus particle assembly from the plasma membrane (PM).
93 teins in virus assembly.IMPORTANCE Influenza virus particle assembly involves the careful coordinatio
94 hermore, defects in NS4A oligomerization and virus particle assembly of two mutants were rescued by N
95 ORTANCE A key aspect in virus replication is virus particle assembly, which is a poorly understood pr
96 nd provides new insights into the process of virus particle assembly.
97 main in coordinating HCV RNA replication and virus particle assembly.
98  each other in some, but not all, aspects of virus particle assembly.
99  the conformation and/or epitope exposure of virus particle-associated ApoE.
100 rental virion only, suggesting a cis-acting, virus particle-associated mechanism of control.
101 A) to a subsequent delay in uncoating of the virus particle at 33 degrees C during the next cycle of
102 of the A17 protein were packaged into mature virus particles at a reduced level, demonstrating that t
103  human immunodeficiency virus type 1 (HIV-1) virus particles at the plasma membrane (PM).
104 the first time direct detection of unlabeled virus particles based on the formation of antibody-virus
105 coded adenovirus proteinase (AVP) before the virus particle becomes infectious.
106  hypothesize that this antibody binds to the virus particle before internalization and endosomal proc
107  structural protein is the primary driver of virus particle biogenesis, and the CA CTD is the primary
108 ntrations of gB-GNP that coat the surface of virus particles block virus entry, whereas lower concent
109          To this end, individual, infectious virus particles bound by fluorescently labeled antibodie
110 tion by increasing the efficiency with which virus particles bud from infected cells and restoring fi
111 this mutant is grown at a lower temperature, virus particles bud from the host cell, but budding arre
112 mation while having limited effects on total virus particle budding.
113  step for immature Gag lattice formation and virus particle budding.
114 ntral role in the intracellular transport of virus particles but also regulate a wider range of proce
115 and the repetitive structure of the original virus particle, but lack infectious genomic material.
116  compensatory mutant strains showed complete virus particles, but these now formed paracrystalline ar
117 efficacy and altered tropism of these coated virus particles by (123)I scintigraphy and to evaluate t
118               RNA synthesis by even a single virus particle can initiate a productive infection.
119                             The interiors of virus particles can encapsulate and protect sensitive co
120 ns resulted in up to 92 and 80% reduction of virus particle capture and trans-infection, respectively
121 ed nanolenses are rapidly formed around each virus particle captured on the substrate using a portabl
122 n retrovirus that assembles intracytoplasmic virus particles, commandeers the cellular factor YB-1, a
123 ing, suggesting that host damage signals and virus particles compete for retrograde transport.
124                                  Icosahedral virus particles constitute paradigms to study self-assem
125 n termination factor eRF1 produces defective virus particles containing 20 times more gRNA.
126         Here we show that inactivated rabies virus particles containing the MERS-CoV S1 protein induc
127                                              Virus particles containing those fusions maintained the
128 is evidently highly specific such that every virus particle contains a set of 10 RNA segments, the or
129                    The resulting fluorescent virus particles could be visualized in virus entry studi
130  lytic replication reduces the production of virus particles, demonstrating the requirement of BBLF1
131 HCPs) were exposed to mainly small influenza virus particles (diameter, <4.7 microm), with concentrat
132 ions that prevented generation of infectious virus particles did not abolish acylation of expressed H
133                             In a fraction of virus particles, EGFP fluorescence was recovered, presum
134 h beta-propiolactone-inactivated recombinant virus particles elicited protective RABV antibody titers
135                                        These virus particles, engineered to selectively bind HSA, ser
136 sponse to low-level stimuli and suggest that virus particle entry is sensed as a stress signal.
137    However, the mechanism by which enveloped virus particle entry mediates a stress response, leading
138 uring fusion, a necessary step for enveloped virus particle entry, appears sufficient to induce trans
139 protein into virus particles, and individual virus particles exhibit brighter red fluorescence.
140 d WSN viruses, scission failed, and emerging virus particles exhibited a "beads-on-a-string" morpholo
141  FEZ1 depletion blocks early infection, with virus particles exhibiting bi-directional motility but n
142 eation of plant-based expression systems and virus particles for use in nanotechnology.
143 s propagation; in its absence, GP-containing virus particles form but are noninfectious, due in part
144 ntiviral effect, since it may interfere with virus particle formation and virus production.
145 ally considered an absolute prerequisite for virus particle formation.
146 tating its interaction with the core for new virus particle formation.
147  three-dimensional reconstruction to analyze virus particles formed by mutants that do not express pa
148 BOR OF BRCA1 (NBR1) targets nonassembled and virus particle-forming capsid proteins to mediate their
149  complex proteins to promote scission of the virus particle from the plasma membrane.
150              Therefore, purified influenza A virus particles from adherent and suspension MDCK host c
151 ced fluorescent detection to separate intact virus particles from DNA and RNA impurities.
152 a corresponding inhibition of the release of virus particles from infected cells.
153 l cells: (i) anterograde axonal transport of virus particles from neuron bodies to axon tips and (ii)
154 ld be less hydrated at pH 5 (where influenza virus particles fuse with endosome membranes) than at pH
155 an at pH 7.4 (where synaptic vesicles or HIV virus particles fuse with plasma membrane).
156    The standard approach for purification of virus particles has been to use a multiple-step, complex
157                                        While virus particles have been observed in M cells, it is not
158                                              Virus particles have been observed within M cells.
159  (HCVcc), it is known that highly infectious virus particles have low to very low buoyant densities.
160 c hippocampal injections of adeno-associated virus particles in APP/PS1 mice, localized primarily to
161 E1 is detrimental to the assembly of Sindbis virus particles in baby hamster kidney cells.
162                    The dynamic properties of virus particles in cells can be imaged by fluorescent pr
163 acellular HCV RNA and accumulates infectious virus particles in cells.
164 ia virus DNA, it can be recovered from these virus particles in enzymatically active form; it is stil
165 ogical entities on Earth, with the number of virus particles in many environments exceeding the numbe
166 c hippocampal injections of adeno-associated virus particles in mutant hAPP Tg mouse brains decreases
167                   Intracellular transport of virus particles in neurons is important, as this process
168 (ORF14) and (ii) ultrastructural features of virus particles in neurons.
169 lar clones replicate better and produce more virus particles in PA28gamma-deficient cells.
170 rmed single-particle tracking of fluorescent virus particles in primary neurons to measure anterograd
171                   Our structures solved from virus particles in solution are largely in agreement wit
172 of computer simulations and experiments with virus particles in tailor-made disk- and annulus-shaped
173 (MMTV) orchestrates the assembly of immature virus particles in the cytoplasm which are subsequently
174  and US9 fail to properly assemble enveloped virus particles in the cytoplasm, which blocks anterogra
175              The tc-VLPs resembled authentic virus particles in their protein composition and neutral
176 ectious virus and RNA-containing hepatitis C virus particles, indicating a block in virus assembly.
177  with JUNV attachment to the cell surface or virus particle internalization into host cells, it preve
178 as viral receptors has enabled insights into virus particle internalization, host and tissue tropism,
179 anisms involved in gE/gI-mediated sorting of virus particles into axons and extracellular spread to a
180 US9 promotes axonal dissemination by sorting virus particles into axons, but whether it is also an ef
181 c domains play important roles in sorting of virus particles into axons.
182 ing both gE and US9 that failed to transport virus particles into axons.
183  detectable SGH(+), or release of detectable virus particles into the blood meals during feeding even
184 measured by the release of newly synthesized virus particles into the cell supernatant.
185 on is dependent on the release of infectious virus particles into the virological synapse.
186 acilitate fluorescence microscopy studies of virus particle intracellular transport, as a brighter pa
187 the assembled lattice of Gag within immature virus particles is necessary to understand the interacti
188               The major product of this, the virus particle, is finding increasing roles in the emerg
189 on, linking viral metagenomic sequences to a virus particle, its sequenced genome, and its host direc
190  spumaviruses; (ii) within the extracellular virus particle itself, transitioning from an RNA-contain
191 siological conditions of one of the simplest virus particles known, the minute virus of mice (MVM) ca
192 ion (V165I) restored polyprotein processing, virus particle maturation, and significant levels of rep
193                            Although multiple virus particles may enter a cell at the same time, mecha
194       HA is the most abundant protein in the virus particle membrane and represents the basis of most
195 lycosphingolipid (GSL) incorporated into the virus particle membrane, as the receptor and ligand for
196  displayed a very good detection limit of 30 virus particles/ml and a wide linear dynamic range of 10
197 und to be 10(4) bacterial cells/mL and 10(4) virus particles/mL, consistent with clinical utility.
198 , when the viremia level had reached 4 log10 virus particles/mL, rescued 100% of Lassa virus-infected
199 mportant in vitro function, which is to make virus particles more infectious, but the mechanism has b
200                Detection limits of 1 x 10(3) virus particles of Human adenovirus C (HAdV), Human astr
201 etection of individual fluorescently labeled virus particles of three influenza A subtypes in two imp
202 imiting HIV-1 endocytosis and in maintaining virus particles on dendrites, which is required for effi
203 interferon-inducible factor tetherin retains virus particles on the surfaces of cells infected with v
204 nts, suggesting that for the majority of the virus particles, only one copy of each RNA segment is pa
205 semen is present in different forms: as free virus particles or as cell-associated virus (ie, within
206 nd virus replication utilize either purified virus particles or deficient genomes that do not complet
207 uired for the efficient production of mature virus particles or serve as a marker for the process.
208 dministration of Ad5.hAC6 (3.2 x 109 to 1012 virus particles) or placebo.
209 rus-like particles, it is not known if these virus particles package and transmit HK2-related sequenc
210 ablish a detection limit of approximately 67 virus particles per milliliter (vp/ml) of EV71 in a Dulb
211 sal adenovirus vaccine doses as low as 10(8) virus particles per mouse induced complete protection ag
212 h HTLV-1 particle populations containing few virus particles possessing a complete capsid core struct
213 us resulted in production of huge amounts of virus particles presenting the peptides all over their s
214  regulating the intracellular trafficking of virus particles prior to nuclear delivery of the viral g
215  receptors recognize genomes within incoming virus particles prior to virus replication.
216 id sensors recognize genomes within incoming virus particles prior to virus replication.
217                                 In contrast, virus particles produced by HSV gE-277 spread poorly to
218 level of GP1,2 expression profoundly affects virus particle production and release and uncovers a new
219 mRNAs bearing tandem RREs (GP-2xRRE), rescue virus particle production in murine cells even in the ab
220 h virus RNA translation in the cytoplasm for virus particle production, and when translation is inhib
221  the actin cytoskeleton severely reduced net virus particle production.
222 ectors to modulate HCV genome replication or virus particle production.
223 s (RNPs), indicating a translational role in virus particle production.
224 relocates sites of assembly, and reduces net virus particle production.
225 y as a powerful and versatile tool to define virus particle profiles.
226                                  Hepatitis D virus particles pseudotyped with surface proteins of U.
227  cellulose particles reduced the influenza A virus particle purification time from 3.5 h to 30 min be
228                                  We employed virus particle purification, genome amplification, pyros
229 duce high titers of VZV, the number of total virus particles relative to the number of viral particle
230 rupting TF production leads to a decrease in virus particle release in both mammalian and insect cell
231 body neutralization of circulating oncolytic virus particles remains a formidable barrier.
232 mers, and incorporation of the proteins into virus particles requires an interaction of Env CT domain
233    Retroviruses first assemble into immature virus particles, requiring interactions between Gag prot
234 sence results in an accumulation of deformed virus particles retaining the scaffold protein and defic
235 electron microscopy analyses of the purified virus particles revealed three classes of particles base
236 nerated heat-sensitive, noninfectious dengue virus particles, revealing a large effect of components
237 neutralizing antibody titer against reporter virus particles (RVPs) representing AA, A1-160K, A1-160Q
238 struct of ZIKV was used to generate reporter virus particles (RVPs) that package a green fluorescent
239                        We then generated the virus particle, self-complementary adeno-associated viru
240 plasma membrane of live cells, and on single virus particles, show the high potential of these dyes f
241 ase, yielding a DNA-containing extracellular virus particle similar to the spumaviruses; (ii) within
242 orly to epithelial cells, despite numbers of virus particles similar to those for HSV gE-348.
243 VP2 is shed from virions in early endosomes, virus particles still consisting of VP5 were trafficked
244 nsitivity of cellular responses to low-level virus particle stimulation, but provide important insigh
245                                We found that virus particles strongly associate with the SM-rich regi
246 ddition, there are defects in the sorting of virus particles such that particles, when formed, do not
247 ppeared to decrease production of infectious virus particles, suggesting a block in virion assembly.
248                                  To do this, virus particles tether themselves to dyneins and kinesin
249 o hairy insects for pollination to nanoscale virus particles that are highly infectious toward host c
250 essfully genetically manipulated to generate virus particles that could be visualized in infected cel
251 ve cell imaging, we show that herpes simplex virus particles that have entered primary human cells ex
252 the envelope glycoprotein (Env) structure on virus particles that is targeted by neutralizing antibod
253                             In addition, the virus particles that were released from cells had reduce
254 sing cryo-electron tomography, we identified virus particles that were spherical, filamentous, and as
255 ity of HIV-1 infections result from a single virus particle (the transmitted/founder) that makes it p
256 ncorporation of the transcription complex in virus particles, the transcriptional activity of A19-def
257 rium dissociation constants such that in the virus particle, they are predicted to be essentially irr
258  antigenically indistinguishable from mature virus particles, they are less stable and readily conver
259                   As symmetry exists in many virus particles, this method may also be applied to 3D s
260 r the first time in any metazoan, infectious virus particles through self-assembly from transgenes.
261 ntous actin, which hints toward transport of virus particles through the use of a myosin motor.
262                      Generation of influenza virus particles thus critically relies on a functional s
263 ividual virion with the capacity of the same virus particle to undergo membrane fusion.
264 on drives the conversion of stable, immature virus particles to a mature, metastable state primed for
265  contained the PM marker, and could transfer virus particles to noninfected cells.
266 apture HIV-1 particles and transfer captured virus particles to T cells without establishing producti
267 roteins that mediate virus attachment tether virus particles to the cell surface, initiating infectio
268  virus release by cross-linking newly formed virus particles to the producing cell.
269 ies of proteins on the surface of individual virus particles.To become infectious, HIV-1 particles un
270                                Extracellular virus particles transmit infection between organisms, bu
271 have proven to be a valuable method to study virus particle transport in living cells.
272                              Immature dengue virus particles undergo a dramatic conformational change
273                      More interestingly, the virus particle underneath the MOF shell can be chemicall
274 IKV C-prM-E cell line that produces reporter virus particles upon transfection with a GFP replicon pl
275      Here we analyse the properties of Junin virus particles using a sensitive flow virometry assay a
276   A method for the purification of influenza virus particles using novel magnetic sulfated cellulose
277 cation of PEDOT nanowires that entrain these virus particles using the lithographically patterned nan
278 s sensing of the genomic RNA within incoming virus particles via cytoplasmic RNA sensors to produce t
279 n substrates in vitro and in vivo in nascent virus particles via one-dimensional diffusion along the
280 retic behavior of complexes between rod-like virus particles (virions) and bivalent antibodies.
281 he multivalent consensus vaccine (1 x 10(10) virus particles (vp)/mouse) induced protective HI titers
282  5 up to more than 2000 peptides on a single virus particle was obtained.
283 s that physical contact between nanorods and virus particles was not required for viral inactivation
284 he transcriptional activity of A19-deficient virus particles was severely reduced.
285 ylated and recruited to the endosomes, where virus particles were located.
286 e defects in assembly of gE(-) US9(-) mutant virus particles were novel because they were neuron spec
287 Observed cores were generally polygonal, and virus particles were on average 115 nm in diameter.
288                           Late-domain mutant virus particles were seen at the uropod in form of buddi
289 om mycelia and RNA from samples enriched for virus particles were sequenced.
290  of total AAV capsid proteins (4.3 femtomole virus particles) were loaded to the autosampler vial.
291 as maintained within both infected cells and virus particles, where N is assembled as RNPs.
292 r infectious genomes, and are packaged as DI virus particles which can be transmitted to susceptible
293 yo-electron microscopy reconstruction of the virus particle, which demonstrated that most structural
294 s based on recombinant vaccine strain rabies virus particles, which concurrently display the protecti
295 t is important for packaging of genomes into virus particles, which constitutes a previously unknown
296  Encapsidated DI-RNAs were incorporated into virus particles, which reduced the infectivity of virus
297                                     Finally, virus particles with primary patient-derived E1-E2 prote
298 ripheral tissue, whereas the second delivers virus particles within nerve fibers to the neural gangli
299 4 colocalization with the newly internalized virus particles within target lymphocytes and found that
300 le additives to slow down the degradation of virus particles would address the problem.

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