ライフサイエンスコーパス: virus entry

1 ion from the HIV-1 envelope membrane reduces virus entry.

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

3 uncoating, a potentially novel mechanism for virus entry.

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

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

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

7 are endocytosed in a process reminiscent to virus entry.

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

9 gies to help characterize early steps during virus entry.

10 ave recently been found to mediate enveloped virus entry.

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

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

13 which membranes can facilitate nonenveloped virus entry.

14 f signaling molecules, macropinocytosis, and virus entry.

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

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

17 pressed S-mediated cell-cell fusion, but not virus entry.

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

19 ies will be functional receptors for Machupo virus entry.

20 n envelope fusion with cell membranes during virus entry.

21 888A-binding site is likely not required for virus entry.

22 mational changes needed for HA stability and virus entry.

23 f this molecule is a critical amino acid for virus entry.

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

25 with the stable peptide effectively blocked virus entry.

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

27 aid the design of strategies for inhibiting virus entry.

28 hance PS receptor-mediated efferocytosis and virus entry.

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

30 reorganization, thereby regulating influenza virus entry.

31 the primary receptor that normally mediates virus entry.

32 implying that the FLs become exposed during virus entry.

33 biological consequences that stretch beyond virus entry.

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

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

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

37 eceptors in supporting S protein binding and virus entry.

38 ll molecules capable of inhibiting influenza virus entry.

39 is exercised through promotion of efficient virus entry.

40 -1 entry and that desmosterol can operate in virus entry.

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

42 ensin-converting enzyme 2 (ACE2), leading to virus entry.

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

44 angements to bring about membrane merger and virus entry.

45 many different functions and is required for virus entry.

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

47 lated in viral particles to ensure efficient virus entry.

48 imes the heterodimer for dissociation during virus entry.

49 signalling molecule folds and implicated in virus entry.

50 tromer has not been previously implicated in virus entry.

51 viral fusion proteins that are critical for virus entry.

52 into the mechanism for IAV uncoating during virus entry.

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

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

55 peptides have been derived as antagonists of virus entry.

56 minant negative VPS4 substantially inhibited virus entry.

57 ly potent small molecule inhibitors of Ebola virus entry.

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

59 ecessary but not sufficient for blocking the virus entry.

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

61 ceptor 1 (hTfR1) as a host cell receptor for virus entry.

62 ycans from the host's plasma membrane during virus entry.

63 adhesion molecule 1a (mCEACAM1a) and mediate virus entry.

64 ystander role for this protein in regulating virus entry.

65 as being essential for receptor binding and virus entry.

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

67 mbrane-embedded virus receptors required for virus entry.

68 discuss implications for receptor-activated virus entry.

69 1 envelope glycoprotein trimer important for virus entry.

70 e for this recently characterized pathway in virus entry.

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

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

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

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

75 Virus entry and assembly both involve vesicle transport

76 SOS Env supported virus entry and cell-cell fusion only after exposure to

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

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

79 residue with a strict conformation, hindered virus entry and conformational changes of the S protein

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

81 of PE and PS maximizes PS receptor-mediated virus entry and efferocytosis and underscore the importa

82 ng the NA surface antigen could also inhibit virus entry and egress to provide host protection.

83 uclear transport, vesicular trafficking, and virus entry and egress.

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

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

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

87 well as for pathogenic processes, including virus entry and Gaucher disease.

88 Ebola GP2 plays a critical role in virus entry and has similarities in mechanism and struct

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

90 ariable UL73/UL74 and RL12/RL13/UL1 loci for virus entry and immunomodulation, but not between genes

91 mall molecule inhibits respiratory syncytial virus entry and infection by blocking the interaction of

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

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

94 lope and host membrane, thereby allowing for virus entry and infection.

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

96 n the ability of the membrane Env to support virus entry and on susceptibility to inhibition by antib

97 formation of stable microtubules soon after virus entry and promote early stages of infection.

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

99 mAb neutralizes virus in vitro by preventing virus entry and spread and is protective in vivo in mous

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

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

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

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

104 ent of the requirement for CD4/CCR5-mediated virus entry and was not observed in CD4+ T cells.

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

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

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

108 Antiviral therapies that impede virus entry are attractive because they act on the first

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

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

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

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

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

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

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

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

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

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

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

120 iroporin from hepatitis C virus (HCV) during virus entry, but also enabled the synthesis of a labelle

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

122 othelial cells induces ROS, which facilitate virus entry by amplifying the infection-induced host cel

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

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

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

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

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

128 provide evidence that promotion of influenza virus entry by glucosylceramidase extends to other endos

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

130 e tetraspanin proteins, facilitate enveloped virus entry by promoting virus-cell membrane fusion.

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

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

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

134 The measles virus entry concert has four movements.

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

136 al sequence diversity, peptides that inhibit virus entry could potentially fulfill the need for new a

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

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

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

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

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

142 During virus entry, Env needs to change shape.

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

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

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

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

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

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

149 , their contribution to receptor binding and virus entry has not been fully investigated.

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

151 REAF is degraded by Vpr within 30 min of virus entry in a manner dependent on the nuclear localiz

152 VCR1) receptor of host cells, which enhances virus entry in cells as well as in brain tissue in vivo.

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

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

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

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

157 These findings reveal a mechanism of virus entry in which receptor engagement and signal tran

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

159 elf, important molecular players involved in virus entry include the tetraspanin CD151 and the epider

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

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

162 of gpTfR1 or hTfR1 comparably enhances JUNV virus entry/infectivity.

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

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

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

166 Virus entry into a host cell provides a conserved target

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

168 is multicapsid nonenveloped virus.IMPORTANCE Virus entry into a susceptible cell is the first step of

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

170 as attributed to the increased efficiency of virus entry into C3A cells.

171 ) trimer of gp120-gp41 heterodimers mediates virus entry into CD4-positive (CD4(+)) cells.

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

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

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

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

176 Virus entry into cells is a multistep process that often

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

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

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

180 P) is a membrane fusion machine required for virus entry into cells.

181 envelope glycoprotein (Env) trimer mediates virus entry into cells.

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

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

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

185 CoV-2 spike (S) glycoprotein trimer mediates virus entry into host cells and cytopathic effects (sync

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

187 r factors that modulate CoV entry.IMPORTANCE Virus entry into host cells is one of the key determinan

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

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

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

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

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

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

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

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

196 e spanning virion glycoprotein essential for virus entry into neuronal axons, virion assembly, and pa

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

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

199 The HIV envelope glycoprotein mediates virus entry into target cells by fusing the virus lipid

200 in EphA2 binding affinity by KSHV.IMPORTANCE Virus entry into target cells is the first step for viru

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

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

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

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

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

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

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

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

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

210 pacity to block HCMV infection by inhibiting virus entry into the host cell.

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

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

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

214 Virus entry is a multistep process.

215 host cell attachment.IMPORTANCE Nonenveloped virus entry is an incompletely understood process.

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 The immune modulatory protein herpes virus entry mediator (HVEM) is one of several cellular r

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

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

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

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

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

231 mmunoinhibitory signaling through the herpes virus entry mediator pathway.

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

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

234 CD160 and BTLA both bind to herpes virus entry mediator.

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

236 2 (HSV-2) subunit antigen vaccines targeting virus entry molecules have failed to prevent genital her

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

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

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

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

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

242 e S2 subunit was not absolutely required for virus entry or syncytium formation, alteration of palmit

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

244 MF275 apparently activates a virus entry pathway parallel to that triggered by CD4 an

245 trategy can serve as a universal tool to map virus entry pathways and uncover key interacting protein

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

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

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

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

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

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

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

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

257 identify valid therapeutic tools to control virus entry, replication, and spread as well as to impai

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

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

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

261 to inhibitors indicates that MF275-activated virus entry requires formation/exposure of the gp41 hept

262 s demonstrate that three ISGs interfere with virus entry, six affect viral transcription/replication,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 ion of ZIKV E is an important determinant of virus entry, tropism and pathogenesis.

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

285 ilar regions in Africa and share features of virus entry: use of cell surface attachment factors, mac

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

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

288 Env proteins mediate virus entry via extensive conformational rearrangements

289 le targets of neutralizing antibodies, drive virus entry via receptor-mediated endocytosis and endoso

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

291 Virus entry was not sufficient to induce HLA upregulatio

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

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

294 identified to function in interference with virus entry, were expressed at significantly higher leve

295 This supports a model for influenza virus entry where cells restrict or permit membrane fusi

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

297 ge the human ACE2 receptor and to facilitate virus entry, which can occur through low-pH-endosomal pa

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

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

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