ライフサイエンスコーパス: virus release

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

2 obtained from 7 different patients enhanced virus release.

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

4 ultivesicular body biogenesis, and enveloped virus release.

5 1 requires its catalytic activity to promote virus release.

6 r complex required for membrane scission and virus release.

7 ing infectivity, viral protein expression or virus release.

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

9 HCV infectivity and lipid droplet-dependent virus release.

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

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

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

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

14 rus production, but some exhibited decreased virus release.

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

16 ine both cellular location and efficiency of virus release.

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

18 tinct CD8 chimeric proteins did not increase virus release.

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

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

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

22 to map the sequences required for efficient virus release.

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

24 ne expression with appropriate kinetics, and virus release.

25 on and further suggest that caspases enhance virus release.

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

27 tion with unknown host machinery involved in virus release.

28 necessary but not sufficient for inhibiting virus release.

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

30 functionally complement Vpu with respect to virus release.

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

32 ible for cleaving the receptor to facilitate virus release.

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

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

35 terplay may delineate a common mechanism for virus release.

36 DD4 E3 ubiquitin ligase family to facilitate virus release.

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

38 es has strong negative effects on infectious virus release.

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

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

41 accounted for by defects in replication and virus release.

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

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

44 host resulting in bacterial cell rupture and virus release.

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

46 secretory pathway that compromises influenza virus release.

47 sponsible for cleaving the receptor to allow virus release.

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

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

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

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

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

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

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

55 luenza virus neuraminidase can contribute to virus release.

56 ectivity and compensated for the inefficient virus release.

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

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

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

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

61 ations independently increased the amount of virus released.

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

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

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

65 64-716 expression significantly inhibited WT virus release and Gag processing and that mutation of th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 The progeny virus released by these cells was infectious.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 Virus released from activated latent cells competes agai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 Virus release in monocyte-derived macrophages was marked

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

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

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

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

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

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

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

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

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

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

173 Enveloped virus release is driven by poorly understood proteins th

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

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

176 Virus release is somewhat delayed by treatment with ammo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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