ライフサイエンスコーパス: infected cell

1 4) and low viral infectivity (<1.5 new cells infected/cell).

2 y allowing Casp8p41 to bind Bak and kill the infected cell.

3 ition of type I interferon production in the infected cell.

4 ment of Chlamydia separate from the original infected cell.

5 that is then integrated into the DNA of the infected cell.

6 L-6, which can be detected in the context of infected cells.

7 insufficient immune-mediated elimination of infected cells.

8 ngly with ADCC-Abs titers against H7N9 virus-infected cells.

9 monomer and protein conjugates rises in HCMV-infected cells.

10 intaining KSHV latent infection in naturally infected cells.

11 r levels of MMP2 and MMP9 activity than mock-infected cells.

12 various interactions both within and between infected cells.

13 expansion and activation, which can destroy infected cells.

14 sufficient to eliminate reactivated latently infected cells.

15 to RSV antigens expressed on the surface of infected cells.

16 expression levels of innate immune genes in infected cells.

17 ate effects on infectious virion egress from infected cells.

18 ith autophagosomes was also confirmed in HCV-infected cells.

19 MPase activity is significantly decreased in infected cells.

20 virus (HIV)-1 reverse transcription in HIV-1-infected cells.

21 ment for detecting exceedingly rare latently infected cells.

22 immune clearance and promote survival in the infected cells.

23 und, which suppressed viral RNA synthesis in infected cells.

24 V-1 assembles at the plasma membrane (PM) of infected cells.

25 odulating Rb family protein function in HCMV-infected cells.

26 izing HIV-1-specific ADCC to eliminate HIV-1-infected cells.

27 and B cells, and direct cytotoxicity against infected cells.

28 2E8 caused complement-mediated lysis in DENV-infected cells.

29 evented the cleavage of viral genomic DNA in infected cells.

30 CVB3 copy number compared with unstimulated infected cells.

31 A3G in a temperature-dependent manner in HPV-infected cells.

32 decreased CD3(+) T cells, and increased SIV-infected cells.

33 lipophagy, but not basal autophagy, in DENV-infected cells.

34 essor of metabolite supply in C. trachomatis-infected cells.

35 dentify HIV RNA-protein interactors in HIV-1 infected cells.

36 , LMP1 blocks IRF5-mediated apoptosis in EBV-infected cells.

37 data concerning the sorting of K15P in KSHV-infected cells.

38 L-12) in HCMV-infected cells but not in mock-infected cells.

39 les and buds at the plasma membrane of virus-infected cells.

40 tion, replication, and genome maintenance in infected cells.

41 the effector functions that target latently infected cells.

42 undercut by the inability to target latently infected cells.

43 ecently appreciated, clonal expansion of HIV-infected cells.

44 ds leads to increased beta-oxidation in DENV-infected cells.

45 abrogated intranuclear filament formation in infected cells.

46 and clearance of herpes simplex virus (HSV1)-infected cells.

47 ins to inhibit the host protein synthesis in infected cells.

48 bsence of actin tails in VPS52KO- or VPS54KO-infected cells.

49 lta prevents E2F1 activation also in non-EBV-infected cells.

50 lymphocyte (CTL) recognition and killing of infected cells.

51 iR-K9 is important for reducing apoptosis in infected cells.

52 ely eliminates dangerous cells such as virus-infected cells.

53 s ALV integration efficiency in vitro and in infected cells.

54 e response (HR), a rapid programmed death of infected cells.

55 ase and PRDX6 in exosomes derived from HIV-1-infected cells.

56 enhanced antibody-mediated clearance of HIV-infected cells.

57 receptor-4 (CXCR4) facilitates migration of infected cells.

58 nctional antibodies that can eliminate HIV-1-infected cells.

59 se II loading onto the HIV-1 promoter in the infected cells.

60 transcription of viral genomes in naturally infected cells.

61 e levels of HIV RNA expression within single infected cells.

62 to cytoplasmic juxtanuclear membranes within infected cells.

63 d has been shown to induce HIV from latently infected cells.

64 the context of direct interactions with HCMV-infected cells.

65 beans were the most effective in killing HIV-infected cells.

66 in turn, led to augmented cell death in the infected cells.

67 nfected cells could activate latent HIV-1 in infected cells.

68 stently maintained in reservoirs of latently infected cells.

69 in a subset of HIV-1 genomes in productively infected cells.

70 id associated and localized to the nuclei of infected cells.

71 ssor Nef on the ADCC susceptibility of HIV-1-infected cells.

72 ment by secreting a soluble form of PD1 from infected cells.

73 by tethering them to the plasma membrane of infected cells.

74 HC class I presentation of viral peptides by infected cells.

75 copy were used to localize and identify KSHV-infected cells.

76 onsistent with their impaired killing of EBV-infected cells.

77 anmo2 mutant to grow and develop normally in infected cells.

78 s and induced KSHV reactivation in naturally infected cells.

79 does not eliminate the reservoir of latently infected cells.

80 estored CD4 expression to the surface of HIV-infected cells.

81 thering, also shows reduced expression in Ld-infected cells.

82 y important to efforts to eradicate latently infected cells.

83 ted and dramatically reduced in level in the infected cells.

84 ent from transmission electron microscopy of infected cells.

85 expressed on the surface of both virions and infected cells.

86 time in part by expansion of the pool of HIV-infected cells.

87 tor functions that specifically targeted HIV-infected cells.

88 how that HSUR2 also base-pairs with mRNAs in infected cells.

89 detect different viral RNA subpopulations in infected cells.

90 are being investigated to eliminate latently infected cells.

91 ed the fates of multiple viral components in infected cells.

92 ly closed circular DNA (cccDNA) in nuclei of infected cells.

93 assembly, or virus egress via budding out of infected cells.

94 r even release of non-vesicular antigen from infected cells.

95 ach other, and they function as a complex in infected cells.

96 between Rab11A and vRNA in the cytoplasm of infected cells.

97 tion of the cRNA replicative intermediate in infected cells.

98 d rearrangement of the actin cytoskeleton in infected cells.

99 unctions as a trap door to eliminate virally infected cells.

100 h non-coding RNAs (called HSURs) in latently infected cells.

101 bind and activate Bak to induce apoptosis of infected cells.

102 entry receptor Nectin-1 from the surface of infected cells.

103 terdepolarizations and triggered activity in infected cells, (2) reduced adrenergically mediated vent

104 on of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells across two in vitro latency models.

105 xpression of US28 on the surface of latently infected cells allows monocytes and their progenitor CD3

106 duce apoptosis of tumor cells and/or virally infected cells, although sparing normal cells, and has b

107 tabolic pathways can both eliminate latently infected cells and block lytic replication, thereby inhi

108 oduce effector functions in response to HCMV-infected cells and can prevent virus spread.

109 al adhesions and maintain cell morphology in infected cells and cells infected with viruses lacking p

110 (TSC2) inhibits lipophagy induction in DENV-infected cells and decreases viral replication.

111 ed with mycobacteria efficiently killing the infected cells and decreasing survival of mycobacteria.

112 re a promising new weapon for elimination of infected cells and eradication of the virus.

113 virus expresses more VP26 fusion protein in infected cells and incorporates more VP26 fusion protein

114 pamycin complex 1 (mTORC1) decreases in DENV-infected cells and is inversely correlated with lipophag

115 STX5 is recruited to the cVAC in infected cells and is required for the efficient product

116 Here we used HCV-infected cells and liver biopsies to study how HCV modul

117 ght into the HCV LVP assembly process within infected cells and offers opportunities for designing an

118 releases progeny viruses from the surface of infected cells and prevents viruses becoming trapped in

119 releases progeny viruses from the surface of infected cells and prevents viruses becoming trapped in

120 against native antigens on persistently HIV-infected cells and recombinant antigens on Env-transfect

121 ants, children and adults against H7N9 virus-infected cells and recombinant hemagglutinin (HA), neura

122 cell survival mechanisms is unique to virus-infected cells and relies on regulation of MCL-1 mitocho

123 ficiency with which virus particles bud from infected cells and restoring filament formation at the i

124 at NSs is mainly localized in the nucleus of infected cells and specifically appears to target the nu

125 om uninfected cells activate latent HIV-1 in infected cells and that true transcriptional latency may

126 bility to deliver cell-killing toxins to HIV-infected cells and to perform other antiviral functions.

127 sses a heterologous HA-tag on the surface of infected cells and virions.

128 Haemocytes take up dsRNA from infected cells and, through endogenous transposon revers

129 thways p38 and JNK were modified in latently infected cells, and activation of p38 and JNK signaling

130 sed on the gene expression levels in the non-infected cells, and demonstrated reasonable performance

131 nhance angiogenesis and dissemination of the infected cells, and interfere with the host immune syste

132 enveloped virions at the plasma membrane in infected cells, and it induces NF-kappaB activity, espec

133 gen expression levels, the percentage of HCV-infected cells, and the PD-1/PD-L1 pathways and has anti

134 tected in supernatants from ICOVIR-15K-cBiTE-infected cells, and the secreted BiTEs bound specificall

135 Viruses isolated from persistently infected cells are highly fusogenic, and this phenotype

136 isms and impact of modulating SG assembly in infected cells are not completely understood.

137 HIV-1 reverse transcription products within infected cells are not well understood.

138 Our previous findings showed that latently infected cells are sensitive to inhibitors of cellular m

139 monstrate that TRAILshort is produced by HIV-infected cells, as well as by uninfected bystander cells

140 e ability of VP1 to properly localize within infected cells at high temperatures, as well as reduced

141 atently infected) T cell when a productively infected cell attempts cell-to-cell transmission of viru

142 We observed that in SBV-infected cells, B23 undergoes a nucleolus-to-nucleoplasm

143 herapeutic strategy for eliminating latently infected cells before haematopoietic stem cell transplan

144 ments, we suggest that the death of latently infected cells brought about by pyroptosis, or to a less

145 act as a true immunity system that saves the infected cell but rather enforces an abortive infection

146 of gp41 made the most effective ITs against infected cells but did not neutralize virus and bound on

147 Nectin-1 is removed from the surface of the infected cells but is retained on the surface of cells t

148 etic cytokine interleukin 12 (IL-12) in HCMV-infected cells but not in mock-infected cells.

149 that in addition to neutralization, lysis of infected cells by Abs can effectively participate in HIV

150 K) cells recognize and kill cancer cells and infected cells by engaging cell surface ligands that are

151 one virion per cell allows identification of infected cells by Gag-GFP expression and directly links

152 Subsequent analyses of HSV-infected cells by immunogold electron microscopy and liv

153 ansion reflects homeostatic proliferation of infected cells by interleukin-7 (IL-7) or antigenic stim

154 suggesting dengue is inhibited in Wolbachia-infected cells by localised cholesterol accumulation.

155 Superinfection of latently infected cells by productive virus could similarly remov

156 und that viral proteins produced by a single infected cell can be detected by an ultrasensitive p24 a

157 how that viral proteins produced by a single infected cell can be detected by the ultrasensitive p24

158 s to reactivate the latent reservoir so that infected cells can be recognized and targeted, with the

159 umulate in a long-lasting manner in Shigella-infected cells, causing subsequent formation of covalent

160 t with constitutive expression of HIV RNA in infected cell clones.

161 oplasmic virus assembly compartment (vAC) of infected cells co-localizing with virus tegument protein

162 for transplant recipients, killing latently infected cells could have far-reaching clinical benefits

163 sting that ATM is proviral in the context of infected cell cultures.

164 Thus the increase of miRNP stability in Ld-infected cells curtails production of proinflammatory cy

165 In infected cells, DBR1 knockdown inhibited detection of fr

166 ces an abortive infection pathway leading to infected cell death with no phage progeny release.

167 on to T cell loss and how quickly abortively infected cells die in vivo, key parameters for a quantit

168 Wolbachia-infected cells display a differential cholesterol profil

169 Dual-infected cells displayed a plasma cell-like gene express

170 ing and monitoring of HIV genomic DNA within infected cells during cytoplasmic transit, nuclear impor

171 roduction of infectious virus from lytically infected cells, each at a different stage of viral repli

172 Nef to fully remove CD4 from the surface of infected cells enhanced their susceptibility to eliminat

173 (i.e., TNF-alpha and IFN-gamma) against EBV-infected cells, enhancing NK cell activation.

174 ming TRAIL resistance, in particular how HIV-infected cells escape immune elimination by the TRAIL:TR

175 sion of TLR5 receptor and agonist in Mobilan-infected cells established an autocrine/paracrine TLR5 s

176 In infected cells, EV71 3A redirects ACBD3, to the replicat

177 ranscripts were increased in wild-type HIV-1-infected cells exposed to purified exosomes from uninfec

178 h G382R and H442Y (G382R/H442Y variant) also infected cells expressing rhesus CD4 with markedly great

179 cAMP triggers premature parasite egress from infected cells followed by serial invasion attempts lead

180 nt cellular cytotoxicity (ADCC) to eliminate infected cells following reactivation from HIV-1 latency

181 Instead, we found that in HCMV-infected cells glucose carbon can be used for lipid synt

182 We tested this approach in HIV-infected cells grown in the lab and in animal infections

183 ural protein produced in large quantities by infected cells, has the characteristics of a viroporin.

184 entiviral and gammaretroviral integration in infected cells have been discovered, but the factors tha

185 In infected cells, HCF-1 was also found to be associated wi

186 Correspondingly, HPV-infected cells heat-treated at 44 degrees C showed accum

187 ndicate that proliferation of these latently infected cells helps maintain the HIV-1 reservoir.

188 s triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8

189 viral glycoprotein D (gD) form a complex in infected cells; (ii) that during infection Nectin-1 is r

190 ve light and electron microscopy analysis of infected cells illustrates that intravacuolar Rab1A vesi

191 lentiviral or gammaretroviral integration in infected cells.IMPORTANCE The majority of human gene the

192 by 75-90% and reduced the overall number of infected cells in dermis by 65%.

193 However, the small numbers of latently infected cells in individuals treated during hyperacute

194 esponse to DNA damage, benefited survival of infected cells in response to a DNA damage response.

195 imals strongly correlated with the number of infected cells in the intestine and plasma viral load.

196 obilized NK cells to eliminate >80% of HIV-1-infected cells in vivo 1 day after its administration.

197 onstrate that cytotoxic ICs can target virus-infected cells in vivo but also highlight potential prob

198 recapitulate the characteristics of latently infected cells in vivo is crucial to identifying and dev

199 better recapitulate the behavior of latently infected cells in vivo This model can be used to study m

200 tential drivers of clonal expansion of HIV-1-infected cells in vivo.

201 (CRISPR)-enzymatically inactive Cas9 in MVM-infected cells increased both cyclin B1 protein and RNA

202 The programmed self-destruction of infected cells is a powerful antimicrobial strategy in m

203 we demonstrate that mTORC1 activity in HSV-1-infected cells is largely insensitive to stress induced

204 thesis of double-stranded RNA (dsRNA) within infected cells is required for necroptosis.

205 fragment with the highest copy number in the infected cells, is derived from Salmonella 5'-leader of

206 rticles produced from a distinct chronically infected cell line are polymorphic in nature, with many

207 inhibition of influenza virus production in infected cell lines (MDCK and A549).

208 ly upregulated in human papillomavirus (HPV)-infected cell lines and tissues.

209 in IT-mediated killing among transfected and infected cell lines that were unrelated to the binding o

210 ry receptor Nectin-1 from the surface of the infected cells may be part of the strategy of the virus

211 nducing the expression of latent HIV so that infected cells may be recognized and eliminated by the i

212 Thus, the proliferation of HIV-1-infected cells may play a role in viral persistence, but

213 In herpes simplex virus (HSV)-infected cells, ND10 bodies assemble at the sites of DNA

214 RVFV pathology is NSs filament formation in infected cell nuclei.

215 l soft x-ray tomography reconstruction of an infected cell nucleus demonstrated that the peripheral,

216 protein (VP1L138P-GFP) (i) in wild-type SA11-infected cells or (ii) in uninfected cells along with vi

217 d phosphoantigens (pAgs) that are present in infected cells or accumulate intracellularly in certain

218 ding protein 1 (ID1) were upregulated in HCV-infected cells or viral core gene-transfected cells.

219 e removal of apoptotic M. tuberculosis (Mtb)-infected cells, or efferocytosis, is considered benefici

220 the minimum number of virions produced by an infected cell over its lifetime is approximately 5,500.

221 iest targets of infection and made up 60% of infected cells over time.

222 To promote virus release from infected cells, pandemic HIV-1 group M strains evolved V

223 es identifies plasma antibody binding to HIV-infected cells, peak ADCC antibody titres, NK cell-media

224 arge and increasing fraction of the residual infected cell population on ART, and insertion of HIV pr

225 hanges the cytokine expression levels within infected cell populations.

226 To counter premature death of a virus-infected cell, poxviruses use a range of different molec

227 e observed vaccine efficacy.IMPORTANCE HIV-1-infected cells presenting Env in the CD4-bound conformat

228 HIV-1-infected cells presenting envelope glycoproteins (Env) i

229 Here we show that HCMV-infected cells produce more glucose-derived pyruvate, wh

230 The immediately early protein of the virus, infected cell protein 0 (ICP0), plays a central role in

231 persensitive to low-energy-induced stress as infected cell protein synthesis and productive replicati

232 roach performed by our novel compound in HIV-infected cells provides a means to bridge the gap betwee

233 equences arose from in vivo proliferation of infected cells, rather than infection of multiple cells

234 Migrating infected cells reactivate from dormancy more than non-mi

235 ral therapy, a persistent reservoir of virus-infected cells remains.

236 ex-1 downregulation and immune escape of HIV-infected cells required for functional interactions with

237 Effective clearance of virally infected cells requires the sequential activity of innat

238 text of infection, and its overexpression in infected cells resulted in decreased levels of both type

239 , venetoclax causes selective killing of HIV-infected cells, resulting in decreased numbers of HIV DN

240 that miR-34 functions through increasing the infected cell's ability to respond to infection through

241 The infected cells showed morphological changes due to struc

242 empty (DNA-less) capsids in the cytoplasm of infected cells, suggesting that UL21 may play a role in

243 6 differentially expressed proteins from RSV-infected cell supernatants were identified at a 1% false

244 -B molecules and downregulates them from the infected cell surface to escape recognition by host cell

245 ells and restoring filament formation at the infected-cell surface.

246 y ET at 5-days post-infection, whereas HIV-1-infected cells surrounded by pools of free virions were

247 massive apoptosis, a small population of HIV-infected cells survive infection, silence viral replicat

248 toxic moiety could function to kill the HIV-infected cells that constitute this reservoir.

249 that creates a cellular environment in virus-infected cells that permits productive virus infection.

250 ize fractional proviral expression in single infected cells that persist despite ART and to assess th

251 n, HIV-1 establishes a reservoir of latently infected cells that persist during antiretroviral therap

252 V integration activity in vitro Likewise, in infected cells, the FACT complex promotes ALV integratio

253 Abundant in stressed or viral-infected cells, the function and potential targets of tR

254 early during infection, whereas in WT virus-infected cells, the majority of the dsRNA was associated

255 toxic T lymphocytes (CTLs) eliminate virally infected cells through directed secretion of specialized

256 tes an endogenous source of cytosolic DNA in infected cells through the release of mitochondrial DNA

257 th specific ligands expressed on tumor/virus-infected cells, thus contributing to immune escape mecha

258 Plant viruses move from the initially infected cell to adjacent cells through plasmodesmata (P

259 osts the ability of CD4mc to sensitize HIV-1-infected cells to ADCC by sera from HIV-1-infected indiv

260 hown to increase the susceptibility of HIV-1-infected cells to ADCC despite the activity of Vpu.

261 e CD4-bound conformation and sensitize HIV-1-infected cells to ADCC mediated by HIV+ sera.

262 therefore reduce the susceptibility of HIV-1-infected cells to ADCC mediated by HIV-positive (HIV+) s

263 s in the enhanced susceptibility of EC HIV-1-infected cells to ADCC responses.IMPORTANCE Attenuated N

264 elated with enhanced susceptibility of HIV-1-infected cells to ADCC.

265 75H/W) increased the susceptibility of HIV-1-infected cells to ADCC.

266 and therefore affects the susceptibility of infected cells to ADCC.

267 and accumulate on the cell surface, allowing infected cells to be detected and targeted by endogenous

268 Short exposure of HCV-infected cells to daclatasvir reduced viral assembly and

269 tate elimination of reactivated latent HIV-1-infected cells to deplete the HIV-1 reservoir and contri

270 itiated from infancy leads to decay of HIV-1-infected cells to exceedingly low concentrations desired

271 enzyme to remodel intracellular membranes of infected cells to set up the functional replication mach

272 uses have evolved multiple ways to adapt the infected cells to their needs, but knowledge about these

273 important for maintaining the attachment of infected cells to their surroundings through modulating

274 Transmission electron micrographs (TEM) of infected cells treated with endocytosis inhibitors showe

275 IRC5 and/or IFI6 was inhibited by shRNA, the infected cells underwent apoptosis rather than pyroptosi

276 sed lytic reactivation of KSHV from latently infected cells upon STAT3 repression with siRNAs or a sm

277 We combined enrichment of HIV-1 infected cells using a reporter virus expressing a surfa

278 Here we analyzed the clonality of HIV-1-infected cells using high-throughput integration site an

279 n to trigger HIV transcription from latently infected cells, via a CDK9/HMBA inducible protein-1 depe

280 ed the dominant mechanism by which the virus-infected cell was thought to undergo programmed cell dea

281 In Zika patients, the frequency of infected cells was lower but the percentage of infected

282 applied low-energy stress, AMPK activity in infected cells was restricted in a Us3-dependent manner.

283 Furthermore, infected cells were cured of PrP(Sc) after exposure of A

284 High titers of ADCC-Abs against H7N9 virus-infected cells were detected in sera from adults and chi

285 Free virions and infected cells were not readily detectable by ET at 5-da

286 lls, and macrophages which internalized dead infected cells were very likely to die themselves, leadi

287 K) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on

288 V is hindered by the persistence of latently infected cells which constitute the viral reservoir.

289 no increase in ICP0 expression in lytically infected cells, which is consistent with the weak expres

290 5,000 virions d(-1)), and the lifetime of an infected cell while producing virus is approximately 5 h

291 TNF response that drives apoptosis of highly infected cells while extending the survival of cells enr

292 m allows H pylori to persist in proximity to infected cells while inducing inflammation only in the n

293 ing immunotherapeutics to clear persistently infected cells will soon allow measurable clinical advan

294 Our data suggest that treatment of infected cells with a STAT3 inhibitor and a viral replic

295 Treatment of CrPV(R146A)-infected cells with actinomycin D, which represses trans

296 ctor receptor (EGFR) from the surface of the infected cells with concomitant suppression of the EGF l

297 med in these plants were small and contained infected cells with disrupted symbiosome membranes, indi

298 mation in melanoma cells caused by fusion of infected cells with many uninfected cells, increased cyt

299 rved distinct EdU puncta in the cytoplasm of infected cells within 12 h postinfection and subsequent

300 ts a possible strategy to eliminate latently infected cells without increasing virion production.