ライフサイエンスコーパス: virus release

1 taneous lytic gene expression and infectious virus release.

2 mplex and bridges the system to HIV-1 Gag in virus release.

3 (gp350) genes, gp350 surface expression, and virus release.

4 ubiquitin ligase (UL) is a critical event in virus release.

5 e disruption of the keratin networks may aid virus release.

6 IV-1 Gag also recruits Nedd4-1 to facilitate virus release.

7 ultivesicular body biogenesis, and enveloped virus release.

8 receptors, and thus facilitated NA-mediated virus release.

9 1 requires its catalytic activity to promote virus release.

10 r complex required for membrane scission and virus release.

11 ing infectivity, viral protein expression or virus release.

12 ication but did affect (cell-type dependent) virus release.

13 rin, which may selectively inhibit cell-free virus release.

14 HCV infectivity and lipid droplet-dependent virus release.

15 ll's budding machinery that are critical for virus release.

16 r Vpu in enhancing HIV-1 and murine leukemia virus release.

17 beta-catenin results in depressed levels of virus release.

18 upporting the notion that NC plays a role in virus release.

19 rus production, but some exhibited decreased virus release.

20 interferes with HIV-1 but not with influenza virus release.

21 ine both cellular location and efficiency of virus release.

22 tion and contains a PPPY motif important for virus release.

23 protease, which cleaves C from prM, allowing virus release.

24 tinct CD8 chimeric proteins did not increase virus release.

25 Vpu is an HIV-encoded protein that enhances virus release.

26 membrane, thus arguing against an effect on virus release.

27 sponsible for cleaving the receptor to allow virus release.

28 ted human cells caused a similar increase in virus release.

29 to map the sequences required for efficient virus release.

30 ne expression with appropriate kinetics, and virus release.

31 on and further suggest that caspases enhance virus release.

32 the lack of Vpu and thereby ensure efficient virus release.

33 tion with unknown host machinery involved in virus release.

34 at a distinct region of Gag is necessary for virus release.

35 functionally complement Vpu with respect to virus release.

36 obtained from 7 different patients enhanced virus release.

37 HEV genome, the ORF3 protein is involved in virus release.

38 sembly, formation of immature particles, and virus release.

39 for lysosomal degradation, thereby blocking virus release.

40 NA synthesis versus nonlytic quasi-enveloped virus release.

41 A, but low levels of unspliced viral RNA and virus release.

42 genital mucosae for infection and subsequent virus release.

43 s most likely abortive, with minimal progeny virus release.

44 a A and B viruses to inhibit NA activity and virus release.

45 s that cannot bind NEDD4L cannot function in virus release.

46 necessary but not sufficient for inhibiting virus release.

47 urface presentation, and inhibition of HIV-1 virus release.

48 ible for cleaving the receptor to facilitate virus release.

49 ovel function for ICP27 in the regulation of virus release.

50 A and a 5-h window between transcription and virus release.

51 terplay may delineate a common mechanism for virus release.

52 DD4 E3 ubiquitin ligase family to facilitate virus release.

53 es has strong negative effects on infectious virus release.

54 sion correlates with the timing and level of virus release.

55 GT 1a-2a chimeric genomes further increased virus release.

56 membrane-associated uORF protein facilitates virus release.

57 accounted for by defects in replication and virus release.

58 uggesting that it may play an active role in virus release.

59 e de novo synthesis of viral DNA and promote virus release.

60 host resulting in bacterial cell rupture and virus release.

61 high variability in the magnitude of initial virus release.

62 l gene expression, and direct restriction of virus release.

63 secretory pathway that compromises influenza virus release.

64 BV L-domain motif is sufficient to stimulate virus release.

65 ST-2/tetherin, a cellular protein inhibiting virus release.

66 in the nuclear membrane leading to lysis and virus release.

67 otif, but not the PREP motif, is involved in virus release.

68 the 74LR mutant are similarly inefficient in virus release.

69 n of the 74LR mutant was not due to improved virus release.

70 ST-2/tetherin, a cellular protein inhibiting virus release.

71 luenza virus neuraminidase can contribute to virus release.

72 ectivity and compensated for the inefficient virus release.

73 ma membrane, which is the site of productive virus release.

74 ations independently increased the amount of virus released.

75 ctivity is separable from the restriction of virus release: a YxY sequence in the cytoplasmic domain

76 d approach to measure antibody inhibition of virus release across a panel of monoclonal antibodies ta

77 Lyn(-/-) cells are impaired in virus release and are rescued when reconstituted with wi

78 This implies that virus release and entry are efficiently coordinated to s

79 ead is more than the sum of the processes of virus release and entry.

80 64-716 expression significantly inhibited WT virus release and Gag processing and that mutation of th

81 HIV-1, as proteasome inhibitors also reduce virus release and Gag processing of HIV-2.

82 n has been shown to play a role in efficient virus release and incorporation of Vpr into virions.

83 and E proteins can affect the efficiency of virus release and infection in a manner that is cell typ

84 in the context of MLV replication to direct virus release and infectious virion production.

85 r, the defects of NC mutants with respect to virus release and infectivity could be complemented by a

86 perties may contribute to the role of NS3 in virus release and may have important implications for pa

87 iating interactions with ESCRT necessary for virus release and report the first evidence of RNA invol

88 These Nef proteins promoted virus release and tetherin downmodulation from the cell

89 ribonucleoprotein (vRNP) nuclear export, and virus release and that specific RTKIs hold promise as no

90 t by blocking enzymatic activity, preventing virus release and transmission.

91 ctivity, and specificity, thereby modulating virus release and virulence, and glycosylation at the ca

92 ta demonstrate that Gag and GagPol assembly, virus release, and autoprocessing are regulated by not o

93 ntributes to enhanced attachment, infection, virus release, and cell death through an undefined CIITA

94 he amount of virus production, extracellular virus release, and cell-type-specific fitness.

95 subverts the host immune system, facilitates virus release, and enhances viral infectivity.

96 hat this leads to simultaneous inhibition of virus release, and immune-mediated elimination of both f

97 ein; the transmembrane domain is critical in virus release, and phosphorylation of the cytoplasmic do

98 d a reduction in the virus titer by blocking virus release, and some affected virus morphology, produ

99 r, which results in increased HIV infection, virus release, and T cell depletion.

100 that inhibits viral replication rather than virus release, and to compare efficacy with the current

101 a global scale the decomposition of benthic viruses releases approximately 37-50 megatons of C per y

102 1) have shown that secondary envelopment and virus release are blocked in mutants deleted for the teg

103 inhibitory effects of TIM-family proteins on virus release are extended to other PS receptors, such a

104 nd that the kinetics of HIV-1 production and virus release are faster in MT-4 than in the other T-cel

105 Thus, the inhibitory effects of A34 on virus release are mediated by SHIP2.

106 H7 CVVs was associated with impeded progeny virus release as a result of strong HA receptor binding

107 ancestral reconstructions, cytotoxicity, and virus release assays.

108 arized epithelial cells; the total amount of virus released at egress sites was slightly increased in

109 t proteasome inactivation slightly decreased virus release (at most a twofold effect), while it did n

110 pase activity delayed cytotoxic activity and virus release but increased the overall virus yield.

111 domain has residual biological activity for virus release but is unable to induce CD4 degradation.

112 such mutations yielded modest reductions of virus release but major effects on viral infectivity.

113 ctive domain important for the regulation of virus release but not CD4 degradation.

114 that is necessary for its ability to enhance virus release but that an alternate mechanism provided b

115 d minimal effect on the amount of infectious virus released but probably enhanced entry into cells.

116 tudies revealed that lack of SLP-76 impaired virus release, but did not affect viral entry, integrati

117 Furthermore, it reduced infectious virus release by 80-90% without affecting virus assembly

118 tudied HIV-1 accessory protein that enhances virus release by antagonizing the host restriction facto

119 Both Vpu and HIV-2 Env enhance virus release by counteracting an innate host-cell block

120 The HIV-1 accessory protein Vpu enhances virus release by counteracting the host restriction fact

121 an antiviral factor that inhibits enveloped virus release by cross-linking newly formed virus partic

122 expressing TSG-F or TSG-3' globally inhibits virus release by disrupting the cellular endosomal sorti

123 st that BST-2 antibody treatment may enhance virus release by inducing a redistribution of BST-2 at t

124 gest that the G-stem budding domain promotes virus release by inducing membrane curvature at sites wh

125 In contrast, inhibition of virus release by NS5A inhibitors was potent and rapid, w

126 t working model proposes that BST-2 inhibits virus release by physically tethering viral particles to

127 host factor that broadly restricts enveloped virus release by tethering budded viral particles to the

128 t working model proposes that Bst-2 inhibits virus release by tethering viral particles to the cell s

129 ken together we conclude that enhancement of virus release by Vpu does not, at least in CEMx174 and H

130 ls infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesicular tr

131 IC were highly infectious for T cells while virus released by cultured B cells was only slightly inf

132 The level of infectious virus released by cultured PBMC after treatment with DAB

133 Moreover, virus released by the uterine epithelial cells shortly a

134 Virus released by these cells was able to infect CD4(+)

135 The progeny virus released by these cells was infectious.

136 ed neurons is problematic, as any infectious virus released can superinfect the cultures.

137 848 and the uncoupler CCCP were applied to a virus-releasing cell line to obtain the same increasing

138 , resulting in fewer actin tails and reduced virus release concomitant with less viral spread.

139 To examine further the cell type-specific virus release defect in HeLa versus T cells, transient h

140 mutations in this sequence imposed profound virus release defects in HeLa cells.

141 V-1 budding; however, the effect of TSG-F on virus release does not require Gag binding.

142 stem, the p6 domain did not appear to affect virus release efficiency but p6 deletions and truncation

143 enerally leads to a significant reduction in virus release efficiency, suggesting that MVBs are a non

144 t significantly affect levels of tetherin or virus release efficiency, we observed that overexpressio

145 an activity that we call the enhancement of virus release (EVR).

146 sidues in NC caused a pronounced decrease in virus release from 293T cells, although NC mutant Gag pr

147 First, it regulates virus release from a post-endoplasmic reticulum (ER) com

148 rt that BST-2 antibody treatment facilitates virus release from BST-2(+) cells by interfering with th

149 Notably, HBV could promote HIV-1 DeltaVpu virus release from BST-2-positive HepG2 hepatoma cells b

150 ll lines but that this was followed by rapid virus release from cells.

151 In fact, the rate of virus release from HeLa cells transfected with a full-le

152 dogenous Bst-2 with respect to its effect on virus release from HeLa cells, T cells, and macrophages.

153 Accurately quantifying virus release from HIV-1-infected cells is central to pr

154 Silencing KIF3A strongly decreased virus release from HIV-1-infected macrophages, leading t

155 Neuraminidase promotes influenza virus release from infected cells and facilitates virus

156 Viroporins have been implicated in promoting virus release from infected cells and in affecting cellu

157 ant IAVs, we show that anti-stem Abs inhibit virus release from infected cells by blocking NA, accoun

158 inant OROV glycoprotein secretion and blocks virus release from infected cells, and VPS4 partly coloc

159 This is due to a significant reduction in virus release from infected cells, as the lack of inters

160 To promote virus release from infected cells, pandemic HIV-1 group

161 ular endosomal sorting machinery and promote virus release from infected cells.

162 ich is a transmembrane protein that inhibits virus release from infected cells.

163 es required for transport (ESCRT) to mediate virus release from infected cells.

164 ection in addition to its role in inhibiting virus release from infected cells.

165 T2) is a transmembrane protein that prevents virus release from infected cells.

166 The site of BCC virus release from polarized cells is, therefore, differ

167 f these motifs may play an important role in virus release from specific cell types and therefore be

168 -destroying activity and thereby facilitates virus release from the cell surface.

169 on in the endoplasmic reticulum and enhances virus release from the cell surface.

170 as adp+ Ad, but the cells lysed more slowly, virus release from the cell was retarded, and the plaque

171 us infections, may facilitate an increase in virus release from the infected cell by minimizing recep

172 known as late domains that promote efficient virus release from the infected cell.

173 Virus released from activated latent cells competes agai

174 cells is further separated into infection by virus released from B cells and virus released from epit

175 infection by virus released from B cells and virus released from epithelial cells.

176 f reactivation by the detection of cell-free virus released from ganglion cells cultured in 96-well p

177 he number of epithelial cells susceptible to virus released from infected B cells, to virus released

178 However, the amount of virus released from infected cells was low.

179 to virus released from infected B cells, to virus released from infected epithelial cells, or random

180 y in HAE, leading to accumulation of nascent virus released from the apical surface between 6 and 24

181 man cells to investigate the capacity of any virus released from the porcine cells to infect human ce

182 differences between the mutant and wild-type viruses released from infected cells.

183 Viruses released from PI cells induced higher cell-to-ce

184 r, additional experiments indicated that the virus release function of pp16 was abolished by the dele

185 ore, this effect occurs independently of the virus release function of the HIV-1 accessory protein Vp

186 ed that the timing of particle formation and virus release had the highest impacts on HIV replication

187 of HCV host factor usage for cell entry and virus release has been explored.

188 AP motif in the C terminus of Gag to promote virus release in HeLa cells, and this budding mechanism

189 l for Gag binding to the plasma membrane and virus release in HeLa cells.

190 d -independent antiviral effects, preventing virus release in human LCLs and abrogating gp350 express

191 amined the kinetics of HIV transcription and virus release in latently infected cells reactivated ex

192 Virus release in monocyte-derived macrophages was marked

193 -reversing agent JQ1 but displayed increased virus release in response to treatment with pladienolide

194 g, targeting of Gag to the PM, and efficient virus release in T cells, which in turn likely promotes

195 ilitates Gag binding to the PM and efficient virus release in T cells.

196 ell surface may also contribute to decreased virus release in the presence of GFP-EH21.

197 izing agent-intended to curb the survival of virus released in aerosols generated from dental procedu

198 ells did not impair HIV-1 Env incorporation, virus release, infectivity, or replication.

199 ntrol subjects.Viral RNA expression and late virus release into supernatant was increased 50- and 7-f

200 with endosomal membranes and thereby blocks virus release into the cytosol.

201 e about 1,200-fold greater than the titer of virus released into the basolateral media.

202 Virus released into the culture media of HCV-infected pr

203 orter gene expression correlated poorly with virus release, intracellular viral RNA levels correlated

204 re we investigated whether NC involvement in virus release is a property specific to HIV-1 or a gener

205 We previously demonstrated that virus release is dependent on the endosomal sorting comp

206 Enveloped virus release is driven by poorly understood proteins th

207 In contrast, regulation of virus release is less specific and not restricted to HIV

208 Thus, the ability to regulate virus release is redundant in AD8 and can be controlled

209 Virus release is somewhat delayed by treatment with ammo

210 n was able to infect human T cell lines, but virus released later did not.

211 Comparing clones with different virus release levels showed that they varied not only in

212 To identify predictors of virus release levels, a previously developed high-throug

213 ected in vitro with the flagellin-expressing virus released low levels of biologically active flagell

214 Nedd4-1 interaction with Gag and function in virus release occur through the Alix-binding LYPX(n)L mo

215 intracellular ORF3 protein accumulation and virus release occurred at the apical membrane of polariz

216 We found that the VCC localization and virus release of HIV-1 are severely impaired upon 5ptase

217 -driving passive degradation of internalized virus, release of immune modulating cytokines and chemok

218 l protein synthesis but rather to a block in virus release or egress.

219 ch encodes two separate proteins to regulate virus release or to mediate viral entry, the HIV-2 Env p

220 hout significantly affecting virus assembly, virus release, or incorporation of Gag-Pol and Env prote

221 gnificant effect on HIV-1 Env incorporation, virus release, or particle infectivity.

222 ur results suggest that initial A36-mediated virus release plays a more important role than A36-drive

223 inhibition acting at different stages of the virus release process.

224 anslation, genome replication, assembly, and virus release processes determines the growth rate of a

225 ced cell death, with long term low levels of virus release progressing through the Golgi apparatus.

226 The two new mutants conserved the enhanced virus release properties of the original isolates; the A

227 and ROD14 Envs controlled the enhancement of virus release (referred to here as Vpu-like) activity.

228 cells from the basolateral surface; however, virus release remains in an apical direction.

229 The ability of CAML to inhibit virus release should illuminate new therapeutic strategi

230 -plaque phenotype and a subsequent defect in virus release similar to a recombinant virus that had F1

231 Consistent with previous reports, virus release spanned four orders of magnitude among clo

232 In agreement with previous reports, virus release spanned over four orders of magnitude with

233 protein drives the budding process, and the virus release step is directed by the late (L) assembly

234 xosomal pathway has been implicated in HIV-1 virus release, suggesting a possible link between these

235 interacts with tetherin, it fails to promote virus release, suggesting that O-Vpu deficiency correlat

236 licated faster, and achieved higher rates of virus release than did 633.

237 AGM cells conferred a strong restriction of virus release that was reversed by Vpu and HIV-2 Env, su

238 , characterized by the absence of infectious virus release, the cessation of virion assembly, and a r

239 Enhanced virus release, therefore, did not compensate for the los

240 The MA mutant 16EK restores virus release through enhanced membrane binding.

241 ciency inhibited Vpu-mediated enhancement of virus release through interfering with the activity of V

242 Influenza virus release was associated with high viral loads in na

243 eous second-site mutants exhibiting enhanced virus release was described previously.

244 Moreover, virus release was earlier in THY-treated cells than in a

245 More efficient virus release was not caused by increased proviral trans

246 dotyped within ecotropic virions; polytropic virus release was profoundly elevated in coinfected cell

247 In both cases, virus release was severely diminished even though NC mut

248 Despite the mutation being in integrase, the virus release was significantly suppressed (P < 0.001).

249 vated in coinfected cells, and the ecotropic virus release was unchanged.

250 HSV-1 genomic DNA, the amount of infectious virus released was reduced approximately 3 logs.

251 Consistent with a role for TSG101 in virus release, we demonstrated that overexpressing the N

252 SMRwt) that blocks exNef secretion and HIV-1 virus release, we identified mortalin as an SMR-specific

253 on, inefficient glycoprotein processing, and virus release were suggested by comparison of ICP34.5 fr

254 tol (GPI) anchor, was sufficient to restrict virus release when presented by the CT/TM regions of a d

255 ApoE knockdown reduced HCMV loads and virus release, whereas overexpressing ApoE hampered HCMV

256 premise: spontaneous mutations that increase virus release will be naturally selected by propagating