ライフサイエンスコーパス: viral envelope

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

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

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

4 hrough direct interaction with PtdSer on the viral envelope.

5 represent the major protein component of the viral envelope.

6 virion assembly and infection, underlies the viral envelope.

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

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

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

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

11 at may impinge on the apparently unperturbed viral envelope.

12 to the perinuclear space to obtain a primary 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 ric fusion glycoprotein (F) displayed on the viral envelope.

17 use of destabilization/disintegration of the viral envelope.

18 rs and higher-order structures that form the viral envelope.

19 omposition and biophysical properties of the viral envelope.

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

21 ormations are selectively recruited into the viral envelope.

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

23 equired for the formation of the icosahedral viral envelope.

24 ing a likely natural conformation of VP24 in 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 via a process of membrane fusion between the viral envelope and a cellular membrane.

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

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

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

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

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

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

36 plex virus (HSV) requires fusion between the viral envelope and host membrane.

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

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

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

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

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

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

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

44 AV to sialylated glycans, fusion between the viral envelope and the host membrane, and the formation

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

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

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

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

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

50 This process disrupts viral envelopes and diminishes infectivity but leaves ce

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

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

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

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

55 interacting with virions, destabilizing the viral envelope, and driving virus aggregation and/or int

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

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

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

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

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

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

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

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

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

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

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

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

68 nome surrounded by the capsid protein, and a viral envelope containing 80 spikes, each a trimer of he

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

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

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

72 Thus, we establish the mechanistic basis of viral envelope disruption by specific tweezers and estab

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

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

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

76 l-to-Leu substitution at position 330 of the viral envelope (E) protein.

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

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

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

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

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

82 brane and directing the incorporation of the viral envelope (Env) glycoprotein into virions.

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

84 The viral envelope (Env) glycoprotein is then recruited to t

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

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

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

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

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

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

91 s infectivity, is mediated by binding of the viral envelope (Env) spike protein to its receptors, CD4

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

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

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

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

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

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

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

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

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

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

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

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

104 e, numerous integrated viral genes including viral envelope genes that are part of LTR retrotransposo

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

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

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

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

109 HIV-1 enters cells through binding between viral envelope glycoprotein (Env) and cellular receptors

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

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

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

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

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

115 y virus type 1 (HIV-1) entry into cells, the viral envelope glycoprotein (Env) trimer [(gp120/gp41)(3

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

117 (HIV-1) entry into cells is mediated by the viral envelope glycoprotein (Env) trimer, which consists

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 ibodies (NAbs) through molecular features of viral envelope glycoprotein E2, including hypervariable

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

141 -1 activity in vitro, both by displacing the viral envelope glycoprotein gp120 from binding to CCR5 a

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

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

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

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

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

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

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

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

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

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

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

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

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

155 rations to achieve greater similarity to the viral envelope glycoprotein spike, potentially increasin

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

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

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

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

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

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

162 s selected for viruses with mutations in the viral envelope glycoprotein, gp41.

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

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

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

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

167 ximal antigenic site within domain II of the viral envelope glycoprotein.

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

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

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

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

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

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

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

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

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

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

178 Viral envelope glycoproteins are important for viral pat

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

180 the data suggest that HSV-1 gC protects the viral envelope glycoproteins essential for entry, includ

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

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

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

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

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

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

187 Unlike other viral envelope glycoproteins, GPC contains a myristoylat

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

189 Glucosidase targets for therapy include viral envelope glycoproteins.

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

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

192 rticles and cells transiently expressing the viral envelope glycoproteins.

193 are transported in axons independently from viral envelope glycoproteins.

194 ixing through active participation of Sendai viral envelope glycoproteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

208 patial organization of these proteins in the viral envelope may contribute.

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

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

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

212 ate the potential of therapies targeting the viral envelope membrane, and oregano oil is a safe suppl

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

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

215 Underneath the viral envelope of influenza virus, matrix protein 1 (M1)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 ence is influenced by the interaction of the viral envelope protein E2 with heparan sulfate (HS) prot

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

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

235 All isolates from recent outbreaks encode a viral envelope protein that is glycosylated, whereas man

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

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

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

239 sts by searching for the accumulation of the viral envelope protein, ZIKV ribonucleic acid (RNA), and

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

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

242 g antibodies elicited by HIV-1 coevolve with viral envelope proteins (Env) in distinctive patterns, i

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

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

245 Viral envelope proteins catalyze this critical membrane

246 119E, and R169P mutations in the S domain of viral envelope proteins impair virion secretion and that

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

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

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

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

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

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

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

254 lowed M1 particle budding without additional viral envelope proteins.

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

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

257 We generated viral envelope sequences from CSF of 3 participants.

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

259 Viral envelope sequences from week 16 and week 42 plasma

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

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

262 nfluence the quaternary configuration of the viral envelope spike.

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

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

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 trimeric hemagglutinin (HA) proteins on its viral envelope that interact with various sialylated gly

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 H in the endosome, the nanodiscs rupture the viral envelope, trapping viral RNAs inside the endolysos

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 By displaying GPCRs in viral envelopes, we fabricated a Virion Display (VirD) a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 on proteins, thereby promoting fusion of the viral envelope with the endosomal 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 virus 5 (PIV5) enters cells by fusion of the viral envelope with the plasma membrane through the conc

298 s lipid-receptor interactions, the fusion of viral envelopes with cellular membranes during endocytos

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