ライフサイエンスコーパス: virus entry

1 and a subsequent increase in CD169-dependent virus entry.

2 mbrane-embedded virus receptors required for virus entry.

3 erstand the role of these sites during Ebola virus entry.

4 1 envelope glycoprotein trimer important for virus entry.

5 with the stable peptide effectively blocked virus entry.

6 ses do not appear to use these receptors for virus entry.

7 aid the design of strategies for inhibiting virus entry.

8 e prM cleavage, maturation of particles, and virus entry.

9 reorganization, thereby regulating influenza virus entry.

10 the primary receptor that normally mediates virus entry.

11 implying that the FLs become exposed during virus entry.

12 biological consequences that stretch beyond virus entry.

13 s this binding activity but does not enhance virus entry.

14 pe cells with a JNK inhibitor did not affect virus entry.

15 rk as homo- and hetero-oligomers to modulate virus entry.

16 eceptors in supporting S protein binding and virus entry.

17 e for this recently characterized pathway in virus entry.

18 ll molecules capable of inhibiting influenza virus entry.

19 is exercised through promotion of efficient virus entry.

20 -1 entry and that desmosterol can operate in virus entry.

21 us is an attractive target for inhibition of virus entry.

22 nd novel approaches to pinpoint the sites of virus entry.

23 angements to bring about membrane merger and virus entry.

24 many different functions and is required for virus entry.

25 nystatin, an inhibitor of caveolin-mediated virus entry.

26 lated in viral particles to ensure efficient virus entry.

27 imes the heterodimer for dissociation during virus entry.

28 tromer has not been previously implicated in virus entry.

29 viral fusion proteins that are critical for virus entry.

30 into the mechanism for IAV uncoating during virus entry.

31 that residues at both sites are critical for virus entry.

32 x virus (HSV), gD plays an essential role in virus entry.

33 tion of cells was at a post-binding stage of virus entry.

34 peptides have been derived as antagonists of virus entry.

35 minant negative VPS4 substantially inhibited virus entry.

36 while only long-term (12-h) treatments block virus entry.

37 ecessary but not sufficient for blocking the virus entry.

38 n myeloid progenitors begins at the point of virus entry.

39 ue 38 previously reported to be critical for virus entry.

40 ctural components of virions and function in virus entry.

41 The cell imposes multiple barriers to virus entry.

42 y ApoB further verified their involvement in virus entry.

43 to identify host factors required for Ebola virus entry.

44 gDDeltaTEV virions caused slightly increased virus entry.

45 and E2 with apolipoproteins in facilitating virus entry.

46 -based receptors (ephrinB2 and ephrinB3) for virus entry.

47 uld still support fusion and thus facilitate virus entry.

48 ded host range proteins acting downstream of virus entry.

49 HCMV binds to cellular integrins to mediate virus entry.

50 ng of antibodies to virions, thus preventing virus entry.

51 nd pathogenesis, many questions remain about virus entry.

52 receptors, CD4 and CCR5/CXCR4, that promote virus entry.

53 rstanding membrane lysis during nonenveloped virus entry.

54 for S protein-mediated cell-cell fusion and virus entry.

55 uncoating, a potentially novel mechanism for virus entry.

56 essential for mediating cell-cell fusion and virus entry.

57 SR-BI, and its lipid transfer activity, for virus entry.

58 cytosis was not involved in THY-1-associated virus entry.

59 are endocytosed in a process reminiscent to virus entry.

60 sphatidylinositol 3-kinase (PI3K)/Akt during virus entry.

61 gies to help characterize early steps during virus entry.

62 discuss implications for receptor-activated virus entry.

63 ave recently been found to mediate enveloped virus entry.

64 tope as an 'antigenic hot spot' critical for virus entry.

65 teolytic cleavage of GP that is required for virus entry.

66 which membranes can facilitate nonenveloped virus entry.

67 f signaling molecules, macropinocytosis, and virus entry.

68 ty lipoprotein (HDL)-mediated enhancement of virus entry.

69 that are susceptible to bat influenza A-like virus entry.

70 (EBOV) attachment and membrane fusion during virus entry.

71 ies will be functional receptors for Machupo virus entry.

72 n envelope fusion with cell membranes during virus entry.

73 888A-binding site is likely not required for virus entry.

74 mational changes needed for HA stability and virus entry.

75 ncovers two competing processes triggered by virus entry: activation of a pore-activated clearance pa

76 mature virions and is expressed in HPCs upon virus entry although its expression at the time of infec

77 tually reinforcing mechanisms (inhibition of virus entry and antibody-mediated killing).

78 e whether mouse cells could be used to study virus entry and antiviral innate immune responses.

79 ce glycoproteins E1 and E2 are essential for virus entry and are targets for neutralizing antibodies.

80 Virus entry and assembly both involve vesicle transport

81 l that has been shown to be important during virus entry and assembly.

82 ded erythroid progenitor cells after initial virus entry and at least partly accounts for the remarka

83 quire the envelope proteins gB and gH/gL for virus entry and cell-cell fusion; herpes simplex virus (

84 served herpesvirus protein with functions in virus entry and cell-cell spread and is a target of neut

85 our results indicate that gB is required for virus entry and cell-to-cell spread of the virus.

86 and cellular membranes and functions during virus entry and cell-to-cell spread.

87 showed the separation of VP2 from VP5 during virus entry and confirmed that while VP2 is shed from vi

88 onsible for cell membrane penetration during virus entry and contains determinants necessary for viru

89 diate receptor binding, membrane fusion, and virus entry and determine host range.

90 such as gB, are said to play major roles in virus entry and egress.

91 esviridae family, likely directed to promote virus entry and endocytosis.

92 y in the highly conserved gp41 that modulate virus entry and escape from HR1 peptide inhibitors.

93 in regulating the efficiency and kinetics of virus entry and fusion with target cells.

94 y shows a new role for TNF-alpha to increase virus entry and highlights the potential for HCV to expl

95 tive glycoprotein conformations required for virus entry and immune evasion, whereas a beta-sandwich

96 virus M2 protein has important roles during virus entry and in the assembly of infectious virus part

97 lpful to develop novel strategies to prevent virus entry and infection.

98 her define the importance of the V3 loop for virus entry and infection.

99 bling functional genomics of hepatitis delta virus entry and infection.

100 tionale for the metal ion requirement during virus entry and infectivity.

101 aining gp120 and gp41 subunits that mediates virus entry and is a major target of broadly neutralizin

102 (HA) surface glycoprotein promotes influenza virus entry and is the key protective antigen in natural

103 of the viral and endosomal membranes during virus entry and is the target of neutralizing antibodies

104 ent Env binding to rhesus CD4 (rhCD4) limits virus entry and replication and could be enhanced by sub

105 e in a variety of animals to offer efficient virus entry and that several Middle Eastern animals are

106 tiviral action appear to include blocking of virus entry and transmission, possibly by targeting the

107 an antigen that induces antibodies to block virus entry and two antigens that induce antibodies that

108 ments suggest a two-step model for Influenza virus entry and uncoating involving low pH in early and

109 rly block to virion production that is after virus entry and uncoating.

110 coupling the roles of viral glycoproteins in virus entry and virion assembly.

111 for efficient membrane fusion events during virus entry and virus spread.

112 irement for human transferrin receptor 1 for virus entry, and the absence of the receptor was propose

113 iruses use multiple glycoproteins to mediate virus entry, and thus communication among these proteins

114 glycoprotein gp120 plays a critical role in virus entry, and thus, its structure is of extreme inter

115 expression, processing, virus incorporation, virus entry, and virus spread.

116 tions of these findings extend to the use of virus entry antagonists, such as protease inhibitors, wh

117 The receptor functions of NTCP and virus entry are blocked, in vitro and in vivo, by Myrclu

118 The natural portals of virus entry are the mucosal surfaces and the skin where

119 olar endocytosis, both established routes of virus entry, are not critical for cellular entry of LACV

120 iral envelope with cellular membranes during virus entry as well as virus-induced cell-to-cell fusion

121 observed in a single-cycle JC53bl-13/TZM-bl virus entry assay median reciprocal 50% inhibitory conce

122 The RSV fusion protein (F) is essential for virus entry because it mediates viral and host membrane

123 ssociated or extracellular processes such as virus entry, blood clotting, antibody-mediated immune re

124 w that residues 412 to 423 are essential for virus entry but not for E2 folding.

125 exes likely function indirectly in influenza virus entry but play direct roles in viral membrane prot

126 function is critical to events shortly after virus entry but prior to viral RNA synthesis/replication

127 es not prevent virus receptor interaction or virus entry but, instead, induces a post-entry block at

128 the Ebola glycoprotein (I544) that enhanced virus entry, but they did not agree in their conclusions

129 nd, moreover, to be a site for inhibition of virus entry by antibodies, small proteins, and small dru

130 These proteins enhance virus entry by binding the phospholipid, PtdSer, present

131 Influenza virus hemagglutinin (HA) mediates virus entry by binding to cell surface receptors and fus

132 gp120 initiates virus entry by binding to host receptors, whereas gp41 m

133 hemagglutinin (HA) envelope protein mediates virus entry by first binding to cell surface receptors a

134 HCMV into certain cell types, contributes to virus entry by macropinocytosis.

135 nd these Abs are concentrated on the path of virus entry by the neonatal FcR in cervical reserve epit

136 d vagina; and 3) concentrated on the path of virus entry by the neonatal FcR in the overlying epithel

137 as a conformational machine that facilitates virus entry by transitioning between prefusion-closed, C

138 yielded dramatically increased EGFR-specific virus entry compared to retargeted virus carrying wild-t

139 The measles virus entry concert has four movements.

140 artially mature West Nile virus (WNV) during virus entry contributes to infectivity.

141 een mouse and human, suggesting that reduced virus entry contributes to lower mouse DC infectivity.

142 Analysis of potential inhibitors of dengue virus entry demonstrated that antibodies and ligands to

143 e show that both HMPV F-mediated binding and virus entry depend upon multiple RGD-binding integrins a

144 While measles virus entry depends on a receptor-binding protein and a

145 cells, indicating that the nectin-mediated B virus entry depends on gD.

146 es, (ii) the determinants of cell-associated virus entry differ from those of soluble virion infectio

147 exposure either prior to infection or after virus entry enabled active B19V replication.

148 ntified phosphatidylserine (PtdSer)-mediated virus entry-enhancing receptors (PVEERs).

149 fied as phosphatidylserine (PtdSer)-mediated virus entry-enhancing receptors (PVEERs).

150 omes was coupled with serial iterations of a virus entry experiment, narrowing 28 candidate proteins

151 ion was inhibited by antibodies against CD81 virus entry factor.

152 urrently available, but studies suggest that virus entry factors can confer virus susceptibility.

153 e the interplay between entry stoichiometry, virus entry fitness, transmission, and susceptibility to

154 n regions of envelope proteins important for virus entry, formation, and recognition by the host immu

155 of ORF7 deletion on VZV replication cycle at virus entry, genome replication, gene expression, capsid

156 uently, the study of virus egress as well as virus entry has focused almost exclusively on the biolog

157 To initiate membrane fusion and virus entry, herpes simplex virus (HSV) gD binds to a ce

158 To model transocular virus entry in a mammalian species, we established a nov

159 L that blocked SARS-CoV and Ebola pseudotype virus entry in human cells.

160 eptor alpha-dystroglycan in avian cells, but virus entry in susceptible species involved a pH-depende

161 s showed normal virus attachment but delayed virus entry in the absence of TRAF2.

162 Analysis of Ebola virus entry in the presence of #3327 allows us to hypoth

163 p mutations alone were sufficient to restore virus entry in the presence of drug, and the accumulatio

164 at human nectin-2 is a target receptor for B virus entry, in addition to the reported receptor human

165 s alpha-defensin inhibited multiple steps of virus entry, including: (i) Env binding to CD4 and corec

166 o binds PtdSer, does not effectively enhance virus entry, indicating that other domains of TIM protei

167 onpermissive myeloid cells from chemical and virus entry induced cell death by up-regulating a key my

168 membrane interaction data of HRC4, a measles virus entry inhibitor peptide, revealing its increased a

169 ortant to study the therapeutic potential of virus entry inhibitors, especially when combined with st

170 ), integrase strand transfer inhibitors, and virus entry inhibitors.

171 Virus entry into a host cell provides a conserved target

172 ges in the retrovirus envelope gene allowing virus entry into a nonpermissive cell.

173 d-brain barrier permeability, which enhanced virus entry into and infection of the brain.

174 Herpes simplex virus 1 (HSV-1) facilitates virus entry into cells and cell-to-cell spread by mediat

175 derable structural rearrangements to mediate virus entry into cells and to evade the host immune resp

176 serine-375 enhanced Env affinity for rhCD4, virus entry into cells bearing rhCD4, and virus replicat

177 an approach of direct observation of Sindbis virus entry into cells by electron microscopy and immuno

178 Virus entry into cells is a multistep process that often

179 bination, gH:KV and gB:S668N enabled primary virus entry into cells that lacked established HSV entry

180 T) of glycoprotein B (gB:NT) enabled primary virus entry into cells that were devoid of typical HSV e

181 evolution of sexual reproduction, enveloped virus entry into cells, and somatic cell fusion.

182 As shown previously, gB730t blocks virus entry into cells, suggesting that gB730t competes

183 P4), the mouse DPP4 homologue does not allow virus entry into cells.

184 , and gH/gL are necessary and sufficient for virus entry into cells.

185 nd UL131 (gH/gL/UL128-131), is essential for virus entry into epithelial cells.

186 nduced during a primary infection facilitate virus entry into Fc receptor-bearing cells during a subs

187 HCV) E2 envelope glycoprotein is crucial for virus entry into hepatocytes.

188 trimer, a membrane-fusing machine, mediates virus entry into host cells and is the sole virus-specif

189 gglutinin (HA) fusion domain is critical for virus entry into host cells by membrane fusion.

190 Here we find that Ebola virus entry into host cells requires the endosomal calci

191 ctivation of NF-kappaB immediately following virus entry into host cells.

192 ith aplaviroc, a small-molecule inhibitor of virus entry into host cells.

193 mmunodeficiency virus type 1 (HIV-1) mediate virus entry into host cells.

194 rane fusion functions that are essential for virus entry into host cells.

195 They block virus entry into host target cells and halt virus transm

196 he trimeric envelope spike of HIV-1 mediates virus entry into human cells.

197 Furthermore, ARM-H prevents virus entry into human T-cells and should therefore be c

198 ctic HCMV vaccine designed to interfere with virus entry into major cell types permissive for viral r

199 Strikingly, virus entry into nTERT cells occurred with unusual rapid

200 onin receptors are required for facilitating virus entry into susceptible cells.

201 le for mediating interactions with CD163 for virus entry into susceptible host cell.

202 fied receptors, specific for B virus, permit virus entry into target cells through gD-independent pat

203 ells into the circulation, and intracellular virus entry into the brain.

204 o intracellular macrophage compartments upon virus entry into the cell.

205 feature of importance both for unrestricted virus entry into the cells and release of newly produced

206 t, for the first time, evidence of influenza virus entry into the CNS via the olfactory route in an i

207 l cord, which are the known sites for rabies virus entry into the CNS, and enhancements in brain deli

208 at infection is blocked at the early step of virus entry into the host cell by retention of the minor

209 grins to enable their clustering and promote virus entry into the host cell.

210 y human virus infection is the prevention of virus entry into the host cell.

211 ular endosomal membranes, thereby preventing virus entry into the host cell.

212 aling molecules as well as in the process of virus entry into the host.

213 l lines, suggesting gD is not required for B virus entry into these cells.

214 r of endosomal acidification greatly reduced virus entry into TRAF2(-/-) MEFs, suggesting that VACV i

215 a well-orchestrated process of nonenveloped virus entry involving autocleavage of the penetration pr

216 Influenza virus entry is mediated by the acidic-pH-induced activat

217 Virus entry is mediated by the glycoprotein complex cons

218 is in cellular trafficking of viruses beyond virus entry is only partially understood.

219 cludex B, a peptide inhibitor of hepatitis B virus entry, is assumed to specifically target NTCP.

220 er, the pathogenesis, including the route of virus entry, is largely unknown.

221 nd containing Trp420, a residue critical for virus entry, is recognized by several broadly neutralizi

222 Virus entry kinetics correlated with observed fitness di

223 Understanding the molecular mechanisms of B virus entry may help in developing rational therapeutic

224 ermore, we carried out assays to examine the virus entry mechanism and concluded that these two mutat

225 ficiency of either BTLA or its ligand herpes virus entry mediator (HVEM) resulted in reduced numbers

226 al in 40% of FL patients, encodes the herpes virus entry mediator (HVEM) which limits T-cell activati

227 The herpes virus entry mediator (HVEM), a member of the tumour-necr

228 In addition, BTLA's ligand, herpes virus entry mediator (HVEM), was found constitutively ex

229 iratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member of the T

230 mediator, blocks the immunoinhibitory herpes virus entry mediator B and T lymphocyte attenuator/CD160

231 ompetes for glycoprotein D binding to herpes virus entry mediator on T cells (TNFSF14)) activates the

232 mmunoinhibitory signaling through the herpes virus entry mediator pathway.

233 competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocy

234 competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocy

235 otein D, which through binding to the herpes virus entry mediator, blocks the immunoinhibitory herpes

236 Our approach is to include a virus entry molecule and add antigens that block HSV-2 i

237 2 (HSV-2) subunit antigen vaccines targeting virus entry molecules have failed to prevent genital her

238 ent, indicating that affinity thresholds for virus entry must be considered in the context of host-ce

239 ights into the pathway of receptor-activated virus entry.Nipah virus causes encephalitis in humans.

240 In the squamous epithelium, we identify virus entry occurring through diffusive percolation, pen

241 We examined the possible role in virus entry of core components of the autophagy machiner

242 on on HIV-1 replication was not dependent on virus entry or coreceptor expression, as vesicular stoma

243 These genes are not required for virus entry or the expression of viral genes.

244 Virus entry pathways are largely defined by the interact

245 s (TEMs), suggesting that TEMs are preferred virus entry portals.

246 nvelope glycoprotein adopts before and after virus entry (prefusion and postfusion conformations, res

247 promote clean non-leaky fusion suitable for virus entry presumably by interaction of the fusion doma

248 This strategy enables pausing the virus entry process at a specific stage and then restart

249 and -2, where gD is a pivotal protein in the virus entry process.

250 ruses, suggesting that a minor alteration in virus entry protein may allow these viruses to use hTfR1

251 essing, unusually extensive for an enveloped virus entry protein, is mediated by cysteine cathepsins,

252 e domain of TIM-1 is essential for enhancing virus entry, provided the protein is still plasma membra

253 necessary for PtdSer-mediated enhancement of virus entry provides a basis for more effective recognit

254 lture of explanted rat ganglia using a novel virus entry proximity ligation assay (VEPLA).

255 rus to the cell surface, the initial step of virus entry, raises questions concerning the kinetics of

256 species and despite expression of functional virus entry receptors, mice are resistant to henipavirus

257 ckground enabled the use of other nectins as virus entry receptors.

258 factor for HCV; however, its implication in virus entry remains unclear.

259 New inhibitors of hepatitis B virus entry, replication, assembly, or secretion and imm

260 have shown they serve critical functions in virus entry, replication, morphogenesis, and immune evas

261 k specific endocytic pathways, we found that virus entry requires dynamin GTPase and membrane cholest

262 ronavirus (SARS-CoV), it has been shown that virus entry requires the endosomal protease cathepsin L;

263 HCVcc) infection that included inhibition of virus entry, RNA and protein expression, and infectious

264 ed a reduction in efficiency and kinetics of virus entry similar to that of the gK-null virus in comp

265 a mutation in E2 potentially has effects on virus entry, spike assembly, or spike maturation.

266 pendent on CD169-mediated enhancement at the virus entry step, a phenomenon phenocopied in HIV-1 infe

267 ty of viruses are inhibited by IFITMs at the virus entry step.

268 hether preassembly reflects a unique measles virus entry strategy, we characterized the protein-prote

269 scent virus particles could be visualized in virus entry studies of both live and fixed cells.

270 ow that PE plays a key role in TIM1-mediated virus entry, suggest that disrupting PE association with

271 (LDL-R) as a hepatocyte surface receptor for virus entry suggested a significant reduction in E1-G ps

272 Our results reveal a new route for virus entry that is specific to keratinocytes, involves

273 s that undergo conformational changes during virus entry that lead to interactions of the capsid or c

274 We also show that after virus entry, the caspase 9 pathway cascade is initiated.

275 During virus entry, the E2/E1 dimer dissociates within the acid

276 ghly specific antigenic recognition to block virus entry, the Fc domain interacts with diverse types

277 During virus entry, the HA protein binds receptors and is trigg

278 binding and internalization during influenza virus entry, the hemagglutinin (HA) protein is triggered

279 domains supporting enhancement of enveloped virus entry, thereby defining the features necessary for

280 (HIV-1) envelope glycoproteins (Env) mediate virus entry through a series of complex conformational c

281 E1 and apolipoproteins, which may facilitate virus entry through LDL-R into mammalian cells.

282 are activated immediately after influenza B virus entry through the endocytic pathway, whereas influ

283 to these receptor-binding proteins to target virus entry to cells expressing a designated receptor.

284 binding to co-receptors and is necessary for virus entry to establish infection.

285 roteins (G and F) that are both required for virus entry to host cells.

286 ed concentration of these Abs on the path of virus entry to inhibit establishment of infected founder

287 direct binding near these critical sites for virus entry to the host cell.

288 the LDLR in the HCV life cycle by comparing virus entry to the mechanism of lipoprotein uptake.

289 Flavonoids 1 and 2 inhibited virus entry up to 45.0% and 78.7% respectively at non-cy

290 ts select for env gene mutations that enable virus entry via drug-bound coreceptor.

291 Understanding the role of lipids in virus entry via endocytosis is impeded by poor accessibi

292 The mechanism of the flavonoid 2 block to virus entry was demonstrated to be by both the direct ac

293 chanism by which each protein contributes to virus entry, we found that stable depletion of Atg16L1 i

294 ous epithelium being an efficient barrier to virus entry, we reveal that HIV-1 can penetrate both int

295 at coat the surface of virus particles block virus entry, whereas lower concentrations block a later

296 previous studies showed that IFITMs modulate virus entry, which is a very early stage in the virus li

297 ection is blocked during the early stages of virus entry, which is likely due to the relatively high

298 occurring mutations at these positions block virus entry while simultaneously preserving iron-uptake

299 caused approximately 32 to 34% reduction of virus entry, while treatment of gDDeltaTEV virions cause

300 , while inhibition of JNK activity decreased virus entry without affecting binding to the cell surfac