ライフサイエンスコーパス: viral entry

1 mmunodeficiency virus type 1 (HIV-1) mediate viral entry.

2 acid for productive membrane penetration and viral entry.

3 stant to HIV infection by blocking R5-tropic viral entry.

4 ort, G-F interactions, cell-cell fusion, and viral entry.

5 in order to maintain its ability to mediate viral entry.

6 utinin-esterase (HE) protein plays a role in viral entry.

7 tors to which viruses bind and which mediate viral entry.

8 an cell and use of that lipid for subsequent viral entry.

9 ication of 2 novel EBOV inhibitors targeting viral entry.

10 this phospholipid mediates phagocytosis and viral entry.

11 inding to HIV-1 gp120 V3 loop and subsequent viral entry.

12 nhibit the virus-cell membrane fusion during viral entry.

13 embrane fusion of HIV-1, an initiate step in viral entry.

14 ized to facilitate trimer disassembly during viral entry.

15 n biosynthesis, the S2' site is cleaved upon viral entry.

16 gents that block phosphatidylserine-mediated viral entry.

17 VAMP8, but not VAMP7, significantly reduces viral entry.

18 -sulfated heparan sulfate (3-OS HS) mediates viral entry.

19 enues of investigation of lipid droplets and viral entry.

20 ively, that specifically inhibit HA-mediated viral entry.

21 or signaling and early actin dynamics during viral entry.

22 of gp41 that are transiently exposed during viral entry.

23 e hydrocarbon tail of cholesterol influences viral entry.

24 hydrophobic surface, membrane insertion, and viral entry.

25 sential for the platforms to function during viral entry.

26 conformations of CCR5 represent a portal for viral entry.

27 CD81 and occludin, to disrupt the process of viral entry.

28 mplexes mediate membrane fusion required for viral entry.

29 rhaps causing steric hindrance that disrupts viral entry.

30 e this, AS601245 and SP600125 both inhibited viral entry.

31 ers intracellular calcium release to promote viral entry.

32 acting serine/threonine kinase 1 (MKNK1), in viral entry.

33 viral envelope and cellular membrane during viral entry.

34 CD4 binding and coreceptor engagement during viral entry.

35 ssible small-animal model to rapidly measure viral entry.

36 nd broadly neutralizing agent at the site of viral entry.

37 lopment are emerging, such as p7 or NS4B and viral entry.

38 lular cholesterol homeostasis and inhibiting viral entry.

39 oundly affects IFITM3-mediated inhibition of viral entry.

40 ts of transiently expressed WT or DN VPS4 on viral entry.

41 ys a critical role in membrane fusion during viral entry.

42 rminated sugars in glycoproteins to initiate viral entry.

43 therapy led to progressively higher rates of viral entry.

44 cted corneal cell cultures were used to test viral entry.

45 tor recruitment and trafficking occur during viral entry.

46 in undifferentiated cells is at the step of viral entry.

47 teins must be revealed within one trimer for viral entry.

48 ulminating in virus-cell membrane fusion and viral entry.

49 r loop (ECL2) in binding gp120 and mediating viral entry.

50 ement for homotypic F and HN interactions in viral entry.

51 outer coat proteins VP4 and VP7 and inhibit viral entry.

52 /gp41)3] induces membrane fusion, leading to viral entry.

53 h inhibits virus-cell membrane fusion during viral entry.

54 rane fusion is critical toward understanding viral entry.

55 a loop and have been proposed to facilitate viral entry.

56 ) is a type I membrane protein that mediates viral entry.

57 mer of gp120/gp41 heterodimers that mediates viral entry.

58 t also in the membrane fusion process during viral entry.

59 the expansion of the capsid associated with viral entry.

60 the CD4-bound conformation are required for viral entry.

61 HIV-1 recognizes CD4(+) T cells and mediates viral entry.

62 suggesting that CD134 (OX40) may facilitate viral entry.

63 esult in virus-host cell membrane fusion and viral entry.

64 host cell receptors to facilitate subsequent viral entry.

65 ciate with lipoproteins, which contribute to viral entry.

66 rus (HPV) capsid protein L2 is essential for viral entry.

67 GPC SSP plays an essential role in mediating viral entry and also contributes to viral virulence in v

68 velope (E) protein is important in mediating viral entry and assembly of progeny virus during cellula

69 distinct steps in the HCV life cycle (i.e., viral entry and assembly).

70 or-induced paramyxovirus F triggering during viral entry and cell-cell fusion.

71 in of Hendra virus is critical for promoting viral entry and cell-to-cell fusion.

72 Treatment with the peptide inhibited viral entry and cell-to-cell spread both in vitro and in

73 lar calcium (Ca2+) stores and contributes to viral entry and cell-to-cell spread.

74 ed with a reduced efficiency of CD4-mediated viral entry and diminished viral replication.

75 actin dynamics that promote higher levels of viral entry and early DNA synthesis in resting memory CD

76 cept that the cortical actin is a barrier to viral entry and early post-entry migration has led to th

77 inidase (HN) protein plays multiple roles in viral entry and egress, including binding to sialic acid

78 en cellular factors and baculoviruses during viral entry and egress.

79 for a better understanding of mechanisms of viral entry and for vaccine design.

80 ly the L529 I544 double mutation compromised viral entry and fusion.

81 s to independently measure the efficiency of viral entry and gene expression in hamster (ldlF) cells

82 s HIV, type 1 (HIV-1) infection by enhancing viral entry and gene expression.

83 production of a natural oxysterol to inhibit viral entry and implicate membrane-modifying oxysterols

84 d on the viral membrane, is required for HIV viral entry and infection.

85 transmembrane TNF-alpha in facilitating the viral entry and integration of HIV-1 into the DNA of ren

86 onsible for receptor interactions leading to viral entry and is a primary target for neutralizing ant

87 directly regulate the CXCR4 receptor during viral entry and is involved in viral DNA synthesis.

88 eracts with the cellular receptor to mediate viral entry and is thought to be the major target for ne

89 he MT-organizing center (MTOC) shortly after viral entry and more pronounced and diffuse MT reorganiz

90 Antibodies that target F can prevent viral entry and reduce disease caused by RSV.

91 hibition and RNA interference of PLD delayed viral entry and reduced viral titers in vitro.

92 uring infection through mechanisms involving viral entry and replication, TGF-beta signalling, low ap

93 ransmembrane protein (IFITM), which inhibits viral entry and replication-have been reported in the pr

94 the endoplasmic reticulum that could impact viral entry and replication.

95 COPD pBECs were susceptible to increased viral entry and replication.

96 the ability of endothelial cells to support viral entry and replication.

97 s antibodies can be associated with impaired viral entry and replication; however, during the course

98 entamer, were evaluated for their effects on viral entry and spread.

99 arrier is likely exploited by CVB to promote viral entry and subsequent egress.

100 ant for activation of membrane fusion during viral entry and that in the absence of a host target mem

101 t extents, can bind to and block GP-mediated viral entry and that of infectious filoviruses.

102 st that EGFR is a key receptor for efficient viral entry and that the ensuing signaling regulates imp

103 in common marmosets operates at the level of viral entry and that this block can be overcome by adapt

104 ing the nuclear pore if added at the time of viral entry and that, when added as late as 8 h postentr

105 however, the role of ROS in early events of viral entry and the induction of signaling has not been

106 as not observed until day 4, suggesting that viral entry and the onset of inflammation in the CNS occ

107 cleaved to (gp120/gp41)3] is the mediator of viral entry and the principal target of humoral immune r

108 ng the expression of IFITM3, which restricts viral entry and thereby blocks early stages of viral pro

109 rotein of influenza plays a critical role in viral entry and thus is an attractive target for inhibit

110 y, and many cellular components required for viral entry and trafficking continue to be revealed.

111 spike (S) protein is the main determinant of viral entry, and although it was previously shown that M

112 (F) protein to activate membrane fusion and viral entry, and cleaving sialic acid from carbohydrate

113 RNA prevented the calcium responses, blocked viral entry, and inhibited plaque formation by 90% compa

114 tion, inhibited HSV-induced calcium release, viral entry, and plaque formation following infection wi

115 tissue, provide evidence for a mechanism of viral entry, and show that a commonly used antibiotic pr

116 nhibited ZIKV infection in vitro by blocking viral entry, and treatment with 25HC reduced viremia and

117 IFITM proteins impede viral entry, and ZMPSTE24 expression is necessary for IF

118 ase required for processing of SARS-S during viral entry; and (iii) SSAA09E3 [N-(9,10-dioxo-9,10-dihy

119 tablishment of a primary infection following viral entry as well as for efficient viral assembly and

120 iction of HCMV infection involves a block of viral entry, as TAg expression prevented the nuclear del

121 Indeed, viral entry assays exhibited a reduction of viral endocy

122 Viral entry assays using HCV pseudoparticles (HCVpps) of

123 nt decrease in infection but did not prevent viral entry at the plasma membrane.

124 that (i) cell-associated viruses can bypass viral entry blocks in most lymphoid cell lines, (ii) the

125 from the increase in viral morphogenesis and viral entry, both phenomena converging toward an increas

126 e, rat) and dogs, transfer of hNTCP supports viral entry but additional host factors are required for

127 ory activity against HSV-2 if present during viral entry but completely blocked plaque formation if p

128 ese HA and NA residues had minimal impact on viral entry but greatly improved viral release from infe

129 MHV-JHM depends not on the spike protein and viral entry but rather on a combination of the structura

130 ered broad-spectrum lead that does not block viral entry but stimulates effector pathways of the inna

131 e show that the ACE2 protein is required for viral entry but that it is not the primary binding site

132 that UVRAG, in concert with C-Vps, regulates viral entry by assembling a specific fusogenic SNARE com

133 that a soluble protein, Gas6, can facilitate viral entry by bridging viral envelope phosphatidylserin

134 fluenza A virus hemagglutinin (HA) initiates viral entry by engaging host receptor sialylated glycans

135 oproteins, E1 and E2, which together mediate viral entry by engaging host receptors and undergoing co

136 ed infectivity of HCV particles and promoted viral entry by increasing the activation and decreasing

137 which targets the fusion peptide and blocks viral entry by inhibiting conformational changes in gp12

138 ER-directed antibodies, such as Z13e1, block viral entry by interacting with Env at a step after CD4

139 al membrane fusion machinery, and neutralize viral entry by targeting a proteolytically primed, fusio

140 nhibitors of SARS-CoV replication that block viral entry by three different mechanisms.

141 most of these sites have important roles in viral entry, cell-cell fusion, G-F interactions, G oligo

142 , we investigated the role of SIV layer 3 in viral entry, cell-to-cell fusion, and CD4 binding.

143 mbranes-that express Axl, Tyro3, and/or TIM1 viral entry cofactors.

144 ggesting that virus-host interactions during viral entry contribute to treatment failure.

145 g HCV entry into hepatocytes, and aspects of viral entry contributing to HCV host tropism.

146 onses by arrayed presentation of a conserved viral entry domain, a strategy that can be applied to ot

147 se a model by which MKNK1 acts to facilitate viral entry downstream of the epidermal growth factor re

148 highly conserved E protein fusion loop block viral entry downstream of virus-cell binding by inhibiti

149 e HIV-1 envelope (Env) glycoprotein mediates viral entry during both cell-free and cell-to-cell infec

150 We further demonstrated that HA-7 inhibited viral entry during postattachment events but not at the

151 to functioning as a mechanism that restricts viral entry/egress or transports RABV particles through

152 spite permissiveness of these cells to HIV-1 viral entry ex vivo.

153 The significance of these findings in the viral entry field extends beyond NiV to other paramyxovi

154 tracellular cholesterol homeostasis to block viral entry, further underscoring the importance of chol

155 We characterized the HIV-1 env viral entry gene from subject-matched macrophage-tropic

156 HSV-1 and measured the outcomes in terms of viral entry, gene and protein expression, viral replicat

157 us-neutralizing antibodies (Abs) directed at viral entry glycoproteins.

158 Thus, UVRAG governs downstream viral entry, highlighting an important pathway capable o

159 n both binding partners decreases fusion and viral entry, highlighting the functional importance of t

160 epitopes are functional ADCC targets during viral entry in an assay format using virion-sensitized t

161 sults suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor vill

162 de evidence that the trimer is essential for viral entry in both fibroblasts and epithelial cells.

163 Viral entry in CIN85-depleted cells was only moderately

164 er, we demonstrate that alpha-toxin promotes viral entry in NHKs.

165 d alphavbeta3 integrin, respectively, during viral entry in order to drive the increase of Mcl-1 and

166 ies (bnAbs) must be active at the portals of viral entry in the gastrointestinal or cervicovaginal tr

167 odel is of considerable utility for studying viral entry in the three-dimensional context of the live

168 An antibody's ability to block viral entry in this in vivo model is a function of its b

169 an interact with the GP1 subunit and mediate viral entry, including alpha-dystroglycan (alphaDG) and

170 Rather, viral entry increased specifically in the hindbrain of I

171 The role of this motif in viral entry, infectivity, and pathogenesis is poorly und

172 Complementing DAAs, viral entry inhibitors have been shown to prevent liver

173 bition that may affect the impact of diverse viral entry inhibitors presently considered for clinical

174 brane fusion, and thus may be useful natural viral entry inhibitors.

175 6 impaired virus release, but did not affect viral entry, integration, and transcription.

176 havirus particles are required for mediating viral entry into a host cell.

177 These residues are sufficient to mediate viral entry into ALV-J nonpermissive cells.

178 hosphatidylinositol 3-kinase (PI3K) mediates viral entry into CD34(+) human progenitor cells (HPCs),

179 1 envelope glycoprotein spike (Env) mediates viral entry into cells by using a spring-loaded mechanis

180 Viral entry into cells is mediated by arenavirus GPC tha

181 n, we took advantage of mutant viruses whose viral entry into cells relies on the uniquely specific i

182 Epstein-Barr virus (EBV) mediates viral entry into cells using four glycoproteins-gB, the

183 or glycoprotein (G), which are critical for viral entry into cells.

184 body binding affected different processes in viral entry into cells.

185 K.219 cells resulted in readily demonstrable viral entry into each cell line; similar observations we

186 omegalovirus (CMV) is a major determinant of viral entry into epithelial and endothelial cells and a

187 Major factors for viral entry into epithelial cells are the localization a

188 nd induced neutralizing antibody, preventing viral entry into epithelial cells, and (vi) GT-DB and TF

189 Membrane fusion is essential for viral entry into host cells and for cell-cell fusion, a

190 irus type 1 (HIV-1) plays a critical role in viral entry into host cells and is a key target for the

191 e a surface-bound glycoprotein that mediates viral entry into host cells and is a primary target for

192 Viral entry into host cells is mediated by membrane prot

193 Viral entry into host cells is the first step of henipav

194 Viral entry into host cells relies on two viral envelope

195 re the surface glycoproteins responsible for viral entry into host cells, the first step in the virus

196 ike protein of MERS-CoV (MERS-S) facilitates viral entry into host cells, which depends on activation

197 cy virus (SIV) envelope spike (Env) mediates viral entry into host cells.

198 at early stages, most likely at the level of viral entry into host cells.

199 s that block this interaction should prevent viral entry into host cells.

200 pathways exist to sense membrane fusion upon viral entry into host cells.

201 The HIV-1 envelope (Env) mediates viral entry into host cells.

202 uptake of lipid soluble vitamins as well as viral entry into host cells.

203 Although HKU4 spike cannot mediate viral entry into human cells, two mutations enabled it t

204 Our studies highlight the complexity of viral entry into human placental trophoblasts and may se

205 macrophages and dendritic cells, can mediate viral entry into mouse CD11b(+) APCs.

206 V pentameric complex (PC) believed to govern viral entry into select cell types, and GP130, an overla

207 Viral entry into TAg-immortalized fibroblasts could larg

208 studies of BASV-G-driven membrane fusion and viral entry into target cells without replication-compet

209 ing the essential elements needed to mediate viral entry into target cells.

210 in novel strategies for therapies preventing viral entry into target host cells.

211 molecules involved in the critical steps of viral entry into the cytoplasm and persistent viral repl

212 It is believed that MVs are required for viral entry into the host, while EVs are responsible for

213 which bind to the glycans and interfere with viral entry into the target cell.

214 dynamic actin cytoskeleton is necessary for viral entry, intracellular migration, and virion release

215 Viral entry is the first step of the life cycle and rece

216 a fluorescent substrate CCF2-AM, we obtained viral entry kinetic curves that correlated with the NiV-

217 y, allowing the proper interpretation of the viral entry kinetic phenotypes.

218 ic phenotypes, validating NiVLPs as suitable viral entry kinetic tools and suggesting overall relativ

219 llowed us the high-throughput measurement of viral entry kinetics, glycoprotein proportions on indivi

220 ll fusion phenotypes generally correlated to viral entry levels.

221 This intricate process of viral entry likely depends on additional yet-to-be-defin

222 se findings identify a novel role for Akt in viral entry, link Akt and calcium signaling, and suggest

223 le of drebrin in HIV infection by modulating viral entry, mainly through the control of actin cytoske

224 the sequence of initial events that lead to viral entry may indicate a new paradigm for understandin

225 gesting that the phosphatidylserine-mediated viral entry mechanism can be shared by various enveloped

226 y viral envelope phosphatidylserine is now a viral entry mechanism generalized to many families of vi

227 The viral entry mechanism is less active and more sensitive

228 tional rearrangements, suggesting a distinct viral entry mechanism.

229 Infection by other viruses employing similar viral entry mechanisms (such as HIV-1 and severe acute r

230 ly blocks these phosphatidylserine-dependent viral entry mechanisms.

231 ns under physiological conditions by masking viral entry mediators on the epithelial glycocalyx.

232 ACV that plays a role in promoting efficient viral entry, most likely via the plasma membrane.

233 pher the signaling pathways activated during viral entry needed for the robust synthesis of Mcl-1 and

234 ycle, including through inhibition of proper viral entry, normal expression of immediate early genes,

235 es that aptamer IBRV-A4 efficiently inhibits viral entry of BoHV-1 in MDBK cells and is therefore a n

236 Rapamycin interferes with viral entry of CCR5 (R5)-tropic HIV and with basal trans

237 CNS neuropathology likely results from late viral entry of virus that has acquired through evolution

238 rmational changes that result in virus-cell (viral entry) or cell-cell (syncytium formation) membrane

239 or more fusion steps in the common endocytic viral entry pathway.

240 mimetic, impaired HSV-induced Ca2+ release, viral entry, plaque formation, and cell-to-cell spread o

241 Inhibition of viral entry plays a crucial role in the control of BoHV-

242 t IFITM proteins have the ability to inhibit viral entry, possibly by modulating the fluidity of cell

243 ew insights into PRRSV-host interactions and viral entry, potentially facilitating development of con

244 important as it reflects the efficacy of the viral entry process and steers the infectivity of HIV-1

245 However, the detailed mechanisms of the viral entry process are still poorly understood.

246 f these techniques has better elucidated the viral entry process of avian sarcoma and leukosis virus

247 nique signaling network generated during the viral entry process stimulates the upregulation of selec

248 Vanitaracin A inhibited the viral entry process with a submicromolar 50% inhibitory

249 as efforts to develop drugs that inhibit the viral entry process.

250 (and perhaps the metastable states of other viral entry proteins) is more dynamic with transient mot

251 nding site interaction that is necessary for viral entry, raising the possibility that viral escape f

252 ohistochemistry, we found that the candidate viral entry receptor AXL is highly expressed by human ra

253 ind that blocking the glia-enriched putative viral entry receptor AXL reduced ZIKV infection of astro

254 the surface of infected cells, including the viral entry receptor CD4 and coreceptors CCR5 and CXCR4.

255 HIV-1 Nef downregulates the viral entry receptor CD4 as well as the coreceptors CCR5

256 he decidua and placenta is then dependent on viral entry receptor expression in these tissues as well

257 While HVEM was first identified as a viral entry receptor for HSV, it is only recently that H

258 ured levels of HCV RNA and expression of the viral entry receptor in brain tissue samples from 10 inf

259 The viral entry receptor Nectin-1 is also internalized durin

260 34 (OX40) has been implicated as a potential viral entry receptor.

261 art due to low plasma membrane expression of viral entry receptors.

262 ng IFN-stimulated genes (ISGs) that modulate viral entry, replication, and assembly.

263 lected contributions to our understanding of viral entry, replication, morphogenesis, egress and prop

264 Viral entry represents a potential multifaceted target f

265 spontaneously downregulate the expression of viral entry restriction factors such as interferon-induc

266 st that the TB1 and TB2 peptides enhance the viral entry step.

267 ed that LY6E promotes membrane fusion of the viral entry step.

268 the development of antiviral drugs targeting viral entry steps but also will lead to the development

269 Time-of-addition, minigenome, and viral entry studies demonstrated that these classes bloc

270 tes substantially to their capacity to block viral entry, suppress viremia, and confer therapeutic ac

271 parent differences include the complexity of viral entry, temporally regulated viral expression, and

272 ols and suggesting overall relatively slower viral entry than cell-cell fusion kinetics.

273 d reveals a previously undescribed aspect of viral entry that may be susceptible to therapeutic inter

274 gene, critical for assembly and budding) and viral entry (the G [attachment] and F [fusion] genes).

275 During viral entry, the C terminus of p12 is required for tethe

276 rangements undergone by the E protein during viral entry, the function of the linker in the DV infect

277 ENV infection by targeting viral binding and viral entry through D2R- and clathrin-associated mechani

278 virus-induced Akt signaling and facilitates viral entry through interactions with gH by activating t

279 envelope protein of influenza virus mediates viral entry through membrane fusion in the acidic enviro

280 or-triggered structural changes that mediate viral entry through membrane fusion.

281 tent newly identified inhibitor class blocks viral entry through specific targeting of the RSV fusion

282 Receptor-mediated viral entry to endothelial/epithelial cells requires a g

283 le pentameric complex, but not gH/gL, blocks viral entry to epithelial cells in culture.

284 of viral and cellular membranes that permits viral entry to infect targeted cells.

285 cts on HSV-1 and HSV-2 infection and impedes viral entry, trafficking of viral proteins, and capsid f

286 They are also involved in viral entry, tumour growth and metastasis and hence are

287 jugates restrict the MNV-1 life cycle at the viral entry/uncoating step.

288 icate the ISG15 pathway in the regulation of viral entry/uncoating.

289 zed vascular endothelial [TIVE] cells), from viral entry until latency establishment.

290 amino acid residues in receptor binding and viral entry using an H5 subtype.

291 ctrum endogenous HIV-1 inhibitor that blocks viral entry via direct interaction with the gp120 envelo

292 ation, while modulating cell-cell fusion and viral entry via multiple mechanisms.

293 Deleting ORF7 did not affect viral entry, viral genome replication, or the expression

294 lease of new particles was also reduced, but viral entry was not affected.

295 lts suggest that the genetic determinants of viral entry were predominantly enriched in the C3, HR1 a

296 HIV-1 gp41 can be potent inhibitors against viral entry when presented in a nonaggregating trimeric

297 The first block is during viral entry, where virions with relatively acid-stable h

298 target for all 4 compounds was the stage of viral entry, which positions the compounds as potentiall

299 HCV envelope glycoproteins E1 and E2 mediate viral entry, with E2 being the main target of neutralizi

300 UpA dinucleotides occurred immediately after viral entry, with incoming virions failing to form repli

301 hem, mutant Y161A showed cell-type-dependent viral entry without obvious defects in HA protein expres