ライフサイエンスコーパス: viral envelope

1 t of short crescent-shaped precursors of the viral envelope.

2 in the variable 1 and 2 (V1V2) region of the viral envelope.

3 ss in infectivity with a perturbation of the viral envelope.

4 hrough direct interaction with PtdSer on the viral envelope.

5 virion assembly and infection, underlies the viral envelope.

6 ctively: the genetic determinant maps to the viral envelope.

7 mini, and E(rns) loosely associates with the viral envelope.

8 f HA protein were also incorporated into the viral envelope.

9 elope, HIV-1 envelope, GBV-C envelope, or no viral envelope.

10 at may impinge on the apparently unperturbed viral envelope.

11 to the perinuclear space to obtain a primary viral envelope.

12 ormations are selectively recruited into the viral envelope.

13 to incorporation of ReAsH-labeled Mtc in the viral envelope.

14 tors of complement activation into their own viral envelope.

15 of Poxviridae that is expressed on the outer viral envelope.

16 use of destabilization/disintegration of the viral envelope.

17 ctions and coevolutionary adaptations in the viral envelope.

18 d and functionally important residues on the viral envelope.

19 ument that lies between the nucleocapsid and viral envelope.

20 resence of more than a dozen proteins on the viral envelope.

21 equired for the formation of the icosahedral viral envelope.

22 ing a likely natural conformation of VP24 in viral envelope.

23 n occurs postentry and is independent of the viral envelope.

24 omposition and biophysical properties of the viral envelope.

25 membrane glycoproteins that are found in the viral envelope(1).

26 depletion of cholesterol from the influenza viral envelope accelerates fusion kinetics even though i

27 lators of complement activity (RCA) into the viral envelope afforded complement resistance, we grew N

28 The viral envelope and 5'-UTR sequences of the lymphotropic

29 abrogated the ability of XCL1 to bind to the viral envelope and block HIV-1 infection; moreover, a lo

30 V-1 infection by binding to the glycosylated viral envelope and blocking cellular entry.

31 mplications of HIV, gp120, forms part of the viral envelope and can be found in the CSF of infected i

32 Viral fusogens mediate the merger of the viral envelope and cellular membrane during viral entry.

33 proteins promote membrane fusion between the viral envelope and host cell membranes, a critical early

34 ation of a fusion (F) protein that fuses the viral envelope and host cell plasma membrane.

35 ate model, viral nucleocapsids devoid of the viral envelope and membrane glycoproteins are transporte

36 were detected in 59%-78% of patients in the viral Envelope and pre-Membrane/Membrane proteins, which

37 ully achieve the fluorescent labeling of the viral envelope and proteins, but not the genome.

38 lso determined that ORF52 resides inside the viral envelope and remains partially associated with cap

39 n beyond merely anchoring the protein in the viral envelope and that it can affect the structures and

40 transition of HA that induces fusion of the viral envelope and the endosomal membrane, and permits t

41 pendent manner facilitates the fusion of the viral envelope and the endosomal membrane.

42 the interaction between glycoproteins on the viral envelope and the major receptor, CD4, and corecept

43 ough endocytosis, or by direct fusion of the viral envelope and the membrane of the host cell.

44 virus (HIV) infection is fusion between the viral envelope and the T-cell membrane, which must invol

45 obe partitions into the lipid bilayer of the viral envelope and upon far UV irradiation reacts select

46 ing of the Pvs25-PvCSP fusion protein on the viral envelope and was highly expressed upon transductio

47 ein layer linked to the inner leaflet of the viral envelope and with local ordering of the glycoprote

48 Fusion between viral envelopes and host cell membranes, which is mediat

49 The application of different viral envelopes and promoters provided a useful approach

50 rs of complement activation (RCA) into their viral envelopes and, as a result, escape antibody-depend

51 ar stomatitis, Rabies, Mokola and Ross River viral envelopes) and self-complementary adeno-associated

52 age of viral proteins, a nick or hole on the viral envelope, and disruption of the virus structure.

53 accine incorporated H at higher rates in the viral envelope, and the other secreted a soluble H prote

54 taining DENV-2 exhibited marked reduction of viral envelope antigen in midguts and salivary glands af

55 equently gained through analyses of isolated viral envelope antigens, host CD4 receptors, and cognate

56 hat the CD is important for formation of the viral envelope by helping mediate fundamental M-M intera

57 envelope engrafted onto the unrelated CAP63 viral envelope (called 63-88C3).

58 how the hemagglutinin lateral density in the viral envelope changes with cholesterol extraction.

59 Upon restoration of viral envelope cholesterol, this spacing once again expa

60 Furthermore, we also show that viral-envelope cholesterol is required for BDV infectivi

61 ifferent binding mode for glycans on the HIV viral envelope compared with the smaller glycans previou

62 eptor/co-receptor complex CD4/CXCR4 with the viral envelope complex gp120/gp41 (Env).

63 resence of more than a dozen proteins on the viral envelope complicates the dissection of the HSV ent

64 ) and other viruses by binding PtdSer on the viral envelope, concentrating virus on the cell surface,

65 ncluding CD59 on the external surface of the viral envelope confers resistance to complement-mediated

66 We find that the viral envelope contains the mammalian LPS-binding factor

67 nown how lipid and protein components of the viral envelope contribute to its mechanical properties.

68 fect on RSV by inducing direct damage to the viral envelope, disrupting viral particles and decreasin

69 ed strains, which may poorly reflect primary viral envelope diversity.

70 at bind to quaternary epitopes formed by the viral envelope (E) protein dimers or higher-order assemb

71 in an N-linked glycosylation site within the viral envelope (E) protein, whereas many isolates of the

72 f neutralizing antibodies that recognize the viral envelope (E) protein.

73 th the development of antibodies against the viral envelope (E) protein.

74 elopment of an antibody response against the viral envelope (E) protein.

75 HMAb 2D22 binds across viral envelope (E) proteins in the dimeric structure, wh

76 contained only the C3 region from the CAP88 viral envelope engrafted onto the unrelated CAP63 viral

77 ve previously shown that interaction between viral envelope (Env) and receptor directs viral assembly

78 Incorporation of the viral envelope (Env) glycoprotein is a critical requirem

79 lso plays a role in the incorporation of the viral envelope (Env) glycoproteins and can influence par

80 neutralizing antibodies (bNAbs) against the viral envelope (Env) glycoproteins gp120 and gp41, but n

81 The incorporation of viral envelope (Env) glycoproteins into nascent particle

82 with which to probe interactions between the viral envelope (Env) protein and CXCR4 and to identify p

83 ent upon mutations within the V3 loop of the viral envelope (Env) protein and was modulated by additi

84 o cells by binding to the HR-1 region of the viral envelope (Env) protein gp41 subunit.

85 s bearing mutations in the HR1 region of the viral envelope (Env) protein.

86 associated with mutations in the stem of the viral envelope (Env) V3 loop, domains outside V3 can als

87 cent common ancestor (MRCA) sequence for the viral envelope (Env) was determined and aligned with 99

88 Independent viral envelope evolution in the brain has been reported,

89 To monitor viral envelope evolution in these two cohorts of monkeys

90 ents the first example of signaling across a viral envelope following receptor binding.

91 a membrane fission event that separates the viral envelope from the cell surface.

92 s, and cell culture-derived HCV that express viral envelopes from patients who have undergone liver t

93 Highly evolved viral envelopes from viruses isolated at late time point

94 Infection initiates when the viral envelope fuses with the host cell membrane in a pr

95 The internalized viral envelope fuses with the macropinocytic membrane, a

96 an analogy to the structure and function of viral envelope fusion proteins.

97 r vectors containing various portions of the viral envelope gene and the 3' long terminal repeat were

98 cific early genetic changes occurring in the viral envelope gene following vaccination using a highly

99 hieved in this study by DNA shuffling of the viral envelope genes from multiple strains.

100 s a unique approach through DNA shuffling of viral envelope genes to attenuate a positive-strand RNA

101 To further evaluate the role of viral envelope glycans in regulating the IFN-alpha/beta

102 Despite the presence of the viral envelope glycoprotein (Env) and CD4 and chemokine

103 t cells starts with interactions between the viral envelope glycoprotein (Env) and cellular CD4 recep

104 The viral envelope glycoprotein (Env) establishes cell-cell

105 HIV entry involves binding of the trimeric viral envelope glycoprotein (Env) gp120/gp41 to cell sur

106 ecreases the exposure of epitopes within the viral envelope glycoprotein (Env) on the surface of infe

107 ntibodies (MAbs) to distinct epitopes on the viral envelope glycoprotein (Env) provides the potential

108 ction to autologous CD4(+) T cells through a viral envelope glycoprotein (Env) receptor- and actin-de

109 Variations in epitope integrity on the viral envelope glycoprotein (Env) trimer and Env reactiv

110 Interaction of the viral envelope glycoprotein (Env) with a specific cellul

111 Abs and bNAbs target the same regions of the viral envelope glycoprotein (Env), but for reasons that

112 The target of HIV-specific NAbs, the viral envelope glycoprotein (Env), is highly variable in

113 introduced at different positions within the viral envelope glycoprotein (Env).

114 e processing and virion incorporation of the viral envelope glycoprotein (Env).

115 likely include a recombinant version of the viral envelope glycoprotein (Env).

116 ralizing antibodies (bnAbs) that bind to the viral envelope glycoprotein (Env).

117 y immunization with recombinant forms of the viral envelope glycoprotein (Env; the target of anti-HIV

118 particles into cellular endosomes, where the viral envelope glycoprotein (GP) catalyzes fusion betwee

119 avirus life cycle is the biosynthesis of the viral envelope glycoprotein (GP) responsible for virus a

120 ically initiated by an interaction between a viral envelope glycoprotein and a host cell receptor.

121 nterpart, dependent on the expression of the viral envelope glycoprotein and are characterized by a p

122 esults from complex interactions between the viral envelope glycoprotein and both CD4 and CCR5, which

123 cells expressing native conformations of the viral envelope glycoprotein and reveals incomplete overl

124 tion of human cells is the processing of the viral envelope glycoprotein by the cellular subtilisin k

125 dings that a single missense mutation in the viral envelope glycoprotein complex (GPC) is responsible

126 ition 427 in the fusion subunit (GP2) of the viral envelope glycoprotein complex (GPC), thereby raisi

127 hat regulates the composition of alternative viral envelope glycoprotein complexes raises the intrigu

128 process is energy-dependent and mediated by viral envelope glycoprotein complexes.

129 ion of cell-specific receptors by one of the viral envelope glycoprotein complexes.

130 rapping of an intermediate conformation of a viral envelope glycoprotein during the fusion process th

131 We analyzed the interaction of apoE with viral envelope glycoprotein E2 and HCV virions by immuno

132 cell entry involves interaction between the viral envelope glycoprotein E2 and the cell surface rece

133 s initiated with a binding event between the viral envelope glycoprotein gp120 and the cellular recep

134 -1 activity in vitro, both by displacing the viral envelope glycoprotein gp120 from binding to CCR5 a

135 s, a process initiated by the binding of the viral envelope glycoprotein gp120 to the cellular CD4 re

136 ection involve the sequential binding of the viral envelope glycoprotein gp120 to the cellular CD4 re

137 entry is initiated by the interaction of the viral envelope glycoprotein gp120 with CD4, and chemokin

138 nteractions, which seem to be independent of viral envelope glycoprotein gp120, are poorly understood

139 ical structures of the glycans on the native viral envelope glycoprotein gp120--as opposed to recombi

140 tic cell associated lectin (DC-SIGN) and the viral envelope glycoprotein gp120.

141 targets B lymphocytes through binding of the viral envelope glycoprotein gp350 to the complement rece

142 ymphocytes in an interaction mediated by the viral envelope glycoprotein gp350.

143 cid substitutions in the cytoplasmic tail of viral envelope glycoprotein gp41 of the neurovirulent vi

144 opic follicles produce IgG Abs reactive with viral envelope glycoprotein gp41 trimers, and these Abs

145 s by binding to a hydrophobic segment of the viral envelope glycoprotein gp41.

146 F also moderately reduced trafficking of the viral envelope glycoprotein GP64 to the plasma membrane

147 ines the role played by integrins and by the viral envelope glycoprotein H in entry and cell-to-cell

148 D81 receptor-binding site (CD81bs) on the E2 viral envelope glycoprotein have been reported previousl

149 We identify the viral envelope glycoprotein M (gM) as having moderate an

150 the arenavirus life cycle, processing of the viral envelope glycoprotein precursor (GPC) by the cellu

151 re reflected in the binding mechanism of the viral envelope glycoprotein to the cell surface receptor

152 ree components: 1) IgG Abs reacting with the viral envelope glycoprotein trimeric gp41; 2) produced b

153 ralizing antibodies and the evolution of the viral envelope glycoprotein were monitored in rhesus mac

154 Viral escape required mutations in the viral envelope glycoprotein which limited the accessibil

155 hting the dynamic and complex nature of this viral envelope glycoprotein, and can serve as a referenc

156 s direct interaction of CXCL4 with the major viral envelope glycoprotein, gp120.

157 cts via direct interaction with the external viral envelope glycoprotein, gp120.

158 virus into the host cell is mediated by the viral envelope glycoprotein, GPC.

159 Protein E, the principal viral envelope glycoprotein, mediates fusion of the vira

160 thy and dead or dying, were taken up through viral envelope glycoprotein-receptor-independent interac

161 imarily the CD4-binding site (CD4-BS) of the viral envelope glycoprotein.

162 ional reconstitution of membrane fusion by a viral envelope glycoprotein.

163 n of MAbs to two independent epitopes on the viral envelope glycoprotein.

164 n a dose-dependent manner, regardless of the viral envelope glycoprotein.

165 irus (HSV) entry through interactions with a viral envelope glycoprotein.

166 rable sites (epitopes) on the surface of the viral envelope glycoprotein.

167 zing Abs targeting conserved epitopes of the viral envelope glycoproteins (Env) are likely required,

168 (HIV-1) entry into cells is mediated by the viral envelope glycoproteins (Env), a trimer of three gp

169 f HIV-1 into target cells is mediated by the viral envelope glycoproteins (Env).

170 Vaccine-elicited antibodies target the viral envelope glycoproteins (Envs) and can potentially

171 the genetic and antigenic variability of the viral envelope glycoproteins (Envs).

172 Viral envelope glycoproteins are important for viral pat

173 s determined by the co-receptor usage of the viral envelope glycoproteins as well as IFITM subcellula

174 lture-derived HCV containing patient-derived viral envelope glycoproteins from 22 HCV variants isolat

175 rived HCV (HCVcc) containing patient-derived viral envelope glycoproteins from 22 HCV variants isolat

176 which occurs only at later stages, after the viral envelope glycoproteins have been expressed to high

177 Despite the known function of viral envelope glycoproteins in catalyzing fusion with c

178 he virus, where most variation occurs in the viral envelope glycoproteins that are the sole targets f

179 ncy virus (HIV) vaccines is the inability of viral envelope glycoproteins to elicit broad and potent

180 Unlike other viral envelope glycoproteins, GPC contains a myristoylat

181 In contrast to other class I viral envelope glycoproteins, the mature GPC complex con

182 Glucosidase targets for therapy include viral envelope glycoproteins.

183 levels comparable to the natural capacity of viral envelope glycoproteins.

184 ated action of the fusion (F) and attachment viral envelope glycoproteins.

185 rticles and cells transiently expressing the viral envelope glycoproteins.

186 ixing through active participation of Sendai viral envelope glycoproteins.

187 are transported in axons independently from viral envelope glycoproteins.

188 alization by antibodies directed against the viral envelope glycoproteins.

189 Viral entry into host cells relies on two viral envelope glycoproteins: the attachment (G) and fus

190 vast majority of paramyxoviruses utilize two viral envelope glycoproteins: the attachment glycoprotei

191 th HIV infection by binding to the sugars of viral-envelope glycoproteins.

192 These include direct defensin targeting of viral envelopes, glycoproteins, and capsids in addition

193 ciated brain injury induced by a CXCR4-using viral envelope gp120.

194 In view of its position on the viral envelope, gp120 is a part of the retrovirus that i

195 ated functional CHIKV glycoproteins into the viral envelope in place of VSV G.

196 fold more concentrated than elsewhere in the viral envelope, indicating specific recruitment to these

197 d rafts are likely to contribute directly to viral envelope integrity and, in the host membrane, may

198 t the hypothesis that the intracellular ASFV viral envelope is composed of a single lipid bilayer.

199 produced uncertainty over whether the inner viral envelope is composed of a single or double lipid b

200 The mechanism(s) of fusion by the viral envelope is largely categorized as either pH-depen

201 We have shown previously that the viral envelope is the genetic determinant of the differe

202 (E) makes up only a small percentage of the viral envelope, it plays an important, as-yet-undefined

203 g-interacting Env tail but not on changes in viral envelope lipid order.

204 In addition, glycans associated with viral envelopes mask important functional domains from t

205 cal sterol-hemagglutinin interactions in the viral envelope may control the rate-limiting step of fus

206 spatial distribution of hemagglutinin on the viral envelope may influence fusion mechanism.

207 by enveloped viruses requires merger of the viral envelope membrane with target cell membranes, resu

208 al segment transmembrane domain (TMD) on the viral envelope membrane.

209 dy, we identify a genetic determinant in the viral envelope (N173) that increases replication and spr

210 reparations indicated that the intracellular viral envelope of ASFV was not significantly different f

211 The recognition by a viral envelope of its cognate host-cell receptor is the

212 ding receptors or attachment factors for the viral envelope of many viruses, including strains of HIV

213 which resulted in changes to the overlapping viral envelope of the hepatitis B surface antigen (sE164

214 ittle is known concerning the effects of the viral envelope on these cells.

215 ovide insight into understanding the role of viral envelope phosphatidylserine in viral infection.

216 Virus binding by viral envelope phosphatidylserine is now a viral entry m

217 Gas6, can facilitate viral entry by bridging viral envelope phosphatidylserine to Axl, a receptor tyr

218 Mutated MFG-E8, which binds viral envelope phosphatidylserine without bridging virus

219 broad antibodies by exposure to the evolving viral envelope population and tested this concept using

220 dy, we observed that during this period, the viral envelope precursor polyprotein accumulated to high

221 al cells, results in the accumulation of the viral envelope precursor polyprotein, leading to the ind

222 Neutralizing antibodies are directed to the viral envelope protein (E) and an accepted correlate of

223 stem drives the transmembrane anchor of the viral envelope protein (E) toward the fusion loop, burie

224 The viral envelope protein (ENV) facilitates the earliest ev

225 Hypervariable region 1 (HVR1) within viral envelope protein 2 (E2) is involved in the usage o

226 to perinuclear, neuronal regions expressing viral envelope protein and the endoplasmic reticulum (ER

227 red membrane fusion reaction mediated by the viral envelope protein E.

228 Recently, the crystal structure of the viral envelope protein E2 region was resolved as well as

229 -azaindole core heterocycles that target the viral envelope protein gp120 has been prepared.

230 It has been shown that the large viral envelope protein limits the intracellular amplific

231 Influenza virus hemagglutinin (HA) is the viral envelope protein that mediates viral attachment to

232 cells requires the sequential engagement of viral envelope protein with CD4 and coreceptor, we propo

233 nown to be determined by the sequence of the viral envelope protein, although the nature of the neuro

234 ated to account for antigenic changes in the viral envelope protein, hemagglutinin (HA).

235 The viral envelope protein, SFFV gp55, forms a complex with

236 of folding instability (BiP binding) of the viral envelope protein.

237 hitosan (chi) to replace the function of the viral envelope protein.

238 ells and point out that interactions between viral envelope proteins and host cell receptors can have

239 lights the fact that interactions of M1 with viral envelope proteins are essential to direct M1 to th

240 this approach, the transmembrane domains of viral envelope proteins are selectively targeted by the

241 Viral envelope proteins catalyze this critical membrane

242 119E, and R169P mutations in the S domain of viral envelope proteins impair virion secretion and that

243 d mixing, but pH-dependent redistribution of viral envelope proteins into the target cell membrane wa

244 For this to occur, the viral envelope proteins must be efficiently targeted to

245 tion activity results for two panels bearing viral envelope proteins representing either an intergeno

246 oteins required specific interactions of the viral envelope proteins with the internal capsid protein

247 rs, blood-clotting components, and even many viral envelope proteins) occurring in almost all eukaryo

248 ve two alternative fates: (i) envelopment by viral envelope proteins, leading to secretion extracellu

249 sed in these analyses differ solely in their viral envelope proteins, suggesting that the block to XM

250 proposals for a general fusion mechanism for viral envelope proteins.

251 lowed M1 particle budding without additional viral envelope proteins.

252 d from recombinant gp120 (present on the HIV viral envelope), providing the first structural data for

253 glutinin (HA) and neuraminidase (NA)] in the viral envelope, resolve the matrix protein layer lining

254 Most seek to suppress the viral envelope's natural tropism while modifying the rec

255 transmitting partner drives this bottleneck, viral envelope sequences from the blood and genital flui

256 Viral envelope sequences from week 16 and week 42 plasma

257 ng trimeric recombinant proteins to identify viral envelope specific clones.

258 However, the number of targets on the viral envelope spike for such antibodies has been limite

259 nfluence the quaternary configuration of the viral envelope spike.

260 by the native configuration of the trimeric viral envelope spike.

261 V3 variable loop on the gp120 subunit of the viral envelope spike.

262 V-1 that targets the CD4 binding site on the viral envelope spike.

263 The observed binding to the viral envelope spikes is the result of specific CD4-gp12

264 ro-oligomers of SSP, GP1, and GP2, forms the viral envelope spikes that mediate receptor recognition

265 We hypothesize that this unusual viral envelope structure results from the extreme curvat

266 ntified novel conformational epitopes on the viral envelope targeted by broadly cross-neutralizing an

267 rophobic portions of the gp41 protein of the viral envelope that contributes to membrane fusion may m

268 e paramyxovirus fusion (F) protein fuses the viral envelope to a cellular membrane.

269 endothelial cells by bridging glycans on the viral envelope to host cell glycoproteins.

270 Unlike several other viral envelopes to which MBL can bind, both recombinant

271 l for protein engineering to construct novel viral envelope variants that can greatly improve the saf

272 Reconstituted Sendai viral envelopes (virosomes) are well recognized for thei

273 The mapping of epitopes on viral envelopes vulnerable to immune evasion will aid in

274 The appearance of the intracellular viral envelope was determined and compared to that of mi

275 ecause the tegument layer between capsid and viral envelope was reduced.

276 Fusion of the viral envelope with a cellular membrane is required for

277 ramyxoviruses enter host cells by fusing the viral envelope with a host cell membrane.

278 cells by the receptor-mediated fusion of the viral envelope with a host cell membrane.

279 se a specialized fusion protein to merge the viral envelope with cell membranes and initiate infectio

280 ll-to-cell spread by mediating fusion of the viral envelope with cellular membranes and fusion of adj

281 complex and regulates membrane fusion of the viral envelope with cellular membranes during virus entr

282 roteinaceous fusion machineries to merge the viral envelope with cellular membranes for infection.

283 acidification, suggesting that fusion of the viral envelope with cellular membranes is a pH-triggered

284 on to the cellular surface and fusion of the viral envelope with cellular membranes.

285 des (FP) play an essential role in fusion of viral envelope with cellular membranes.

286 molecule and prevents membrane fusion of the viral envelope with cellular membranes.

287 FP is the critical mediator of fusion of the viral envelope with host cell membranes leading to virus

288 on (F) protein, which leads to merger of the viral envelope with target cell membranes.

289 Fusion of the cholesterol-enriched viral envelope with the cell membrane marks the beginnin

290 receptor binding, followed by fusion of the viral envelope with the cell membrane.

291 roteins is required to mediate fusion of the viral envelope with the cell membrane.

292 on proteins, thereby promoting fusion of the viral envelope with the endosomal membrane.

293 fusion protein (F) to mediate merger of the viral envelope with the host cell membrane.

294 matitis virus (VSV G) mediates fusion of the viral envelope with the host cell, with the conformation

295 ught to be central in the membrane fusion of viral envelope with the host membrane.

296 trimeric fusion protein (F) that merges the viral envelope with the plasma membrane at neutral pH.

297 s, whereas the domain required for fusion of viral envelope with the plasma membrane is at the C term

298 virus 5 (PIV5) enters cells by fusion of the viral envelope with the plasma membrane through the conc

299 endosomes, possibly inhibiting the fusion of viral envelopes with endosomal membranes during primary

300 n incomplete shell of density underlying the viral envelope, with a hexagonal honeycomb structure sim