ライフサイエンスコーパス: infected cell

1 tion of Env on the surface of a virion or an infected cell.

2 tosol often without overt destruction of the infected cell.

3 uence protein degradation kinetics within an infected cell.

4 gen(s) displayed by MR1 on the surface of an infected cell.

5 contributes to the destruction of the virus-infected cell.

6 roenvironment for viral RNA synthesis in the infected cell.

7 ittingly exposing new vulnerabilities in the infected cell.

8 activation and interferon production by the infected cell.

9 s and promotes accelerated cell death in HSV-infected cells.

10 thereby further enhancing HSV-1 egress from infected cells.

11 and US9 from transfected cells than those of infected cells.

12 nduce NF-kappaB-dependent gene expression in infected cells.

13 and regulates cell cycle progression in HIV-infected cells.

14 verall state of ISGylation in wild-type (WT)-infected cells.

15 significantly decreased upon aggregation in infected cells.

16 l six passages, comparable with that for 22L-infected cells.

17 oing viral replication and initial number of infected cells.

18 ular bacterial persistence or replication in infected cells.

19 genomes leads to increased death in latently infected cells.

20 perturbed only after long-term culturing of infected cells.

21 p in cytotoxic T cell function, the death of infected cells.

22 unctional disassembly of the capsid shell in infected cells.

23 release of newly formed virus particles from infected cells.

24 to promote immune-mediated clearance of HIV-infected cells.

25 ted elimination of both free virus and virus-infected cells.

26 virus particles from the plasma membranes of infected cells.

27 because existing drugs do not eradicate HIV-infected cells.

28 omplex and leads to loss of cell polarity of infected cells.

29 ividual variation in host responses to clear infected cells.

30 secretion and fail to invade and egress from infected cells.

31 inly in non-infected cells surrounding HSV-1-infected cells.

32 lel pathways of necroptosis and apoptosis in infected cells.

33 te cytokines and viral ligands to kill virus-infected cells.

34 M resulted in increased HIV transcription in infected cells.

35 s and results in a latency-like state in the infected cells.

36 targets the surface of free virus and viral-infected cells.

37 nd enhances motility and invasiveness of the infected cells.

38 rol were rapidly trafficked to ehrlichiae in infected cells.

39 kinase-dependent manner in LXA4-treated KSHV-infected cells.

40 elease failed to reduce PSGL-1 on surface of infected cells.

41 and promotes virus reactivation of latently infected cells.

42 nduces lipid droplet biogenesis in rotavirus-infected cells.

43 dies seeking to eliminate persistently HIV-1-infected cells.

44 roptosis are mutually exclusive fates in IAV-infected cells.

45 treatment reduces the proliferation of HIV-1-infected cells.

46 ing CD4 and BST-2/tetherin on the surface of infected cells.

47 ction between A33 and A34 can be detected in infected cells.

48 ntegrate their genomes into the telomeres of infected cells.

49 rough the presence of viral nucleic acids in infected cells.

50 cting antigen-specific CD8 T cell-killing of infected cells.

51 sibly through phagocytosis of virus or virus-infected cells.

52 at this can occur in EBV-negative and in EBV-infected cells.

53 bility of the immune system to eliminate the infected cells.

54 PR-ubiquitinated host proteins in Legionella-infected cells.

55 measurable reductions in the frequencies of infected cells.

56 stence of a long-lived reservoir of latently infected cells.

57 is confirmed the presence of large clones of infected cells.

58 ecause of a persistent reservoir of latently infected cells.

59 reduced deISGylation in vitro and in porcine-infected cells.

60 l destruction and limited drug delivery into infected cells.

61 tive stress, inflammation, and cell death in infected cells.

62 ere evaluated for the ability to detect FFPE infected cells.

63 pathway's role in regulating YAP/TAZ in ZIKV-infected cells.

64 pseudokinase (MLKL)-dependent necroptosis in infected cells.

65 to be LXA4-interacting host proteins in KSHV-infected cells.

66 dding of viral particles from the surface of infected cells.

67 l replication compartments in the cytosol of infected cells.

68 ere observed in the medium as well as in the infected cells.

69 ubstantially restored in the HVT-DeltavNr-13-infected cells.

70 dimensional structure of the human genome in infected cells.

71 ar nucleotides that are released by dying or infected cells.

72 hedgehog (hh) signaling in LXA4-treated KSHV-infected cells.

73 y early formation of a reservoir of latently infected cells.

74 ction, the in vivo proliferation of latently infected cells.

75 lation of dsRNA and the IFN response in JUNV-infected cells.

76 loit Src family kinases (SFKs) for exit from infected cells.

77 y LXA4 secretion to maintain KSHV latency in infected cells.

78 vitro and fates of viral core components in infected cells.

79 the activation of innate immune signaling in infected cells.

80 N RNA in the cytoplasm compared to wild-type-infected cells.

81 V particles are released from the surface of infected cells.

82 to enhance immune-mediated clearance of HIV-infected cells.

83 erating inclusion bodies in the cytoplasm of infected cells.

84 ) that accompanies higher HPSE expression in infected cells.

85 sal followed by immune-mediated clearance of infected cells.

86 ses 24 virally encoded sncRNA (VZVsncRNA) in infected cells.

87 2 (Day 7 in 4 of 5 participants), mean %HCV-infected cells = 1.0% (95% CI, 0.2%-1.7%) (P < .05 for c

88 earance of viruses and subsequent killing of infected cells(1-4).

89 n but lower capacity to respond to human CMV-infected cells; 2) term pregnancy dNK are not skewed tow

90 At liver biopsy 1, mean %HCV-infected cells = 25.2% (95% confidence interval [CI], 7.

91 more common (35.8%) than those found in RSV-infected cells (4.4%).

92 reviously identified two forms of NSP2 in RV-infected cells, a cytoplasmically dispersed form (dNSP2)

93 al cells, and hematopoietic cells, with some infected cells able to transfer infection.

94 In HMPV-infected cells, actin-based filamentous extensions were

95 Methanol and paraformaldehyde incubation of infected cells also inactivated the virus.

96 EBERs), allowing rapid identification of EBV-infected cells among PBMCs.

97 replication of pathogens by eliminating the infected cell and additionally contributes to the releas

98 that H(2)S/RSS impacts bacterial survival in infected cells and animals.

99 nst pathogens through direct cytotoxicity of infected cells and are the predominant immune cell at th

100 nd limits IAV spread by directly eliminating infected cells and by mobilizing both innate and adaptiv

101 ls are cytotoxic lymphocytes targeting virus-infected cells and cancer cells.

102 ocyte antigen (HLA) class I molecules of MuV-infected cells and characterized by advanced mass spectr

103 endoribonuclease that is activated in virus-infected cells and cleaves single-stranded viral and cel

104 ntified here could serve as markers for KSHV-infected cells and could potentially serve as therapeuti

105 T cells in order to eliminate a majority of infected cells and eradicate briskly spreading HSV-2 inf

106 the ExoN motif, dsRNA readily accumulated in infected cells and often colocalized with dsRNA sensors.

107 wed Abeta42-immunoreactivity mainly in HSV-1-infected cells and only rarely in uninfected cells or in

108 ount a response to curb virus replication in infected cells and prevent spread of virus to neighborin

109 binders, restrict SARS-CoV-2 replication in infected cells and provide a global map of their direct

110 trate co-transport of Rab11A and IAV vRNA in infected cells and provide direct evidence that vRNA-ass

111 ment and persistence of the pool of latently infected cells and review the current approaches aimed a

112 ceptibility to infection, the persistence of infected cells and the establishment of latency.

113 effectively block NK cell targeting of virus-infected cells and the major histocompatibility complex

114 proteins in the cytoplasm and nuclei of NiV-infected cells and thus provides first evidence that IBp

115 enable them to replicate and persist in the infected cells and to evade/modulate the immune response

116 Last, metabolic reprogramming of infected cells and viral lysis alter nutrient cycling an

117 mposed of immune cells surrounding bacteria, infected cells, and a caseous necrotic core.

118 surface CD107a, proliferation, cytolysis of infected cells, and suppression of viral replication.

119 luding the lifespans of short and long-lived infected cells, and the time to reach viral suppression

120 cles, CD9-positive exosomes released from PV-infected cells are also infectious and transport virions

121 We find that infected cells are apolipoprotein- and ACE2-expressing c

122 ell functions important for clearing virally infected cells are impaired by higher negative regulator

123 that facilitate HIV replication in latently infected cells are known.

124 hanisms that contribute to HSV-1 egress from infected cells are poorly understood.

125 Barr virus (EBV) genomes persist in latently infected cells as extrachromosomal episomes that attach

126 In addition to using native virus infected cells as positive control material, the evaluat

127 ately supports the inflammatory breakdown of infected cells at later time points.

128 activity and O-GlcNAcylation is disrupted in infected cells because host hexosamine biosynthesis is b

129 They also show that HCMV-infected cells become resistant to TGF-beta signaling th

130 ubiquitin-proteasome pathway in productively infected cells, before latency establishment and after r

131 significantly reduced cell viability in MDV-infected cells, both glutamine and glucose were required

132 Furthermore, HVT blocks apoptosis in infected cells but activates apoptosis in noninfected by

133 eplication and promotes immune escape of HIV-infected cells but lacks intrinsic enzymatic activity.

134 itation of gE/gI and US9 was observed in HSV-infected cells but not in transfected cells, which argue

135 as markedly different from that of F13-HA in infected cells, but MC021-HA was still incorporated in t

136 ISG-15 mRNA was prominent near infected cells, but not in infected cells, supporting th

137 fic Trm cells predicted rapid elimination of infected cells, but our data suggest that such Trm cell

138 We characterized the persistently infected cells by detecting virus particles, protein and

139 ocus on deflecting CD8 T cell recognition of infected cells by disrupting antigen presentation pathwa

140 b, may be important for early recognition of infected cells by MAIT cells in the lung.

141 s the potential to enable the elimination of infected cells by redirecting endogenous non-HBV-specifi

142 t HCMV decreases the expression of HLA-DR in infected cells by reducing the transcription of HLA-DR t

143 a mammalian orthoreovirus in cryo-preserved infected cells, by cryo-electron tomography of cellular

144 During inflammation, stressed or infected cells can release adenosine triphosphate (ATP)

145 rticles, it has also been suggested that HCV-infected cells can secrete HCV RNA carrying exosomes tha

146 tiple CD4(+) T cell subsets, suggesting that infected cells can undergo T cell differentiation.

147 As latently infected cells cannot be phenotyped directly, the featur

148 We find a rapid transcriptomic change in infected cells, characterized by a shift to an inflammat

149 Some large infected cell clones detected by QVOA carried neutraliza

150 gy is abortive infection (Abi), in which the infected cell commits suicide before the phage can compl

151 panied by enhanced CTL-mediated clearance of infected cells comparable to genetic deletion of Nef.

152 MICB*002 with B44 supertype alleles on DENV-infected cells confer a protective advantage in controll

153 Apical secretions from infected cells contained increased amounts of proteins a

154 pite effective antiretroviral therapy, HIV-1-infected cells continue to produce viral antigens and in

155 Proportions of EBV-infected cells correlated with blood EBV loads.

156 bilize latency and allow immune clearance of infected cells could lead to treatment-free remission.

157 h the establishment of a unique persistently infected cell culture model to study MERS-CoV-bat intera

158 In RSV- or HMPV-infected cells, cytosolic inclusion bodies containing th

159 While data in infected cells demonstrate Cp binding to the proposed ge

160 tes to mount responses to cancer and virally-infected cells, dendritic cells must capture antigens pr

161 MDV-infected cells do not produce infectious cell-free virus

162 ional RNA/DNA hybrids (R-loops) that form in infected cells during S-phase as a consequence of beta-A

163 Within infected cells, EBOV downregulates STAT1 mRNA and interf

164 onditional fluorophore and laser excitation, infected cells emitted green fluorescence that correlate

165 ntly, the transfer of EVs purified from HCMV-infected cells enhanced virus spread.

166 rs resulted in increased specific killing of infected cells, even with neutralization-resistant virus

167 ery from exosomes of hepatitis A virus (HAV)-infected cells (exo-HAV) by clathrin-mediated endocytosi

168 However, not every latently infected cell exposed to a lytic trigger turns on the ex

169 cells and only rarely in uninfected cells or infected cells exposed to antivirals.

170 tive control material, the evaluation of non-infected cells expressing coronavirus (SARS, MERS) spike

171 otein redirects T cells to specifically lyse infected cells expressing the target virus-derived pepti

172 nter, and NPCs are infected via contact with infected cells far more efficiently than by cell-free vi

173 still unknown how astrovirus particles exit infected cells following replication.

174 we show that Can GPC aggregates in the ER of infected cells, forming incorrect cross-chain disulfide

175 uses assemble their replication complexes in infected cells from a multidomain replication polyprotei

176 is used as a mechanism to remove bacterially infected cells from the body.

177 Therefore, EBV BGLF2 might protect virus-infected cells from the type I interferon response in ce

178 the JCI, Chaillon and coworkers assessed HIV-infected cells from various anatomic compartments obtain

179 Tissue-associated HIV-infected cells had different properties than cells in th

180 we analyze the TCR repertoire of single HIV-infected cells harboring translation-competent proviruse

181 protein PfEMP-1 was significantly reduced in infected cells heterozygous for PIEZO1 756del, a phenome

182 In pathogen-infected cells, HLA class I expression is perturbed.

183 eplicate almost entirely in the cytoplasm of infected cells; however, how these pathogens are able to

184 important immunomodulatory complexes within infected cells.IMPORTANCE Many viruses replicate almost

185 fluenza outcomes, recognizes influenza virus-infected cells in a high mannose-dependent manner.

186 uncleaved HA trimers exist on the surface of infected cells in a highly dynamic state that exposes hi

187 CD103(+) CD4(+) T cells are enriched for HIV-infected cells in a latent-like state.

188 nation eliminated reactivated latently HIV-1-infected cells in an ex vivo quantitative viral outgrowt

189 + CD4+ T cells accounted for the majority of infected cells in rectal tissue.

190 Notably, we detected VZV- and HCMV-infected cells in the contralateral, uninoculated xenogr

191 is that the virus can hide in the genome of infected cells in the form of latent proviral DNA.

192 ate that glutamine uptake is elevated by MDV-infected cells in vitro Although glutamine, but not gluc

193 restore the adaptive immune response to HIV-infected cells in vitro and have the potential to enhanc

194 DART molecules were not capable of clearing infected cells in vivo, attributed to the lack of quanti

195 py structure of native gB recovered from VZV-infected cells, in complex with a human monoclonal antib

196 were detected, yet only supernatant from VZV-infected cells induced amylin aggregation and, to a less

197 Efficient viral egress from infected cells is an important step for HSV-1 transmissi

198 control Mtb growth, leading to bacteria and infected cells leaving the granuloma and disseminating,

199 In this study, EBV-infected cell lines derived from gastric cancers and Bur

200 The HDV-infected cell loss was estimated to be 0.052 [0.035-0.07

201 een groups following stimulation with an EBV-infected cell lysate.

202 e quaking-induced conversion assays with RML-infected cell lysates, we observed a strong signal over

203 o proteins interacted with the P. falciparum-infected cell lysates.

204 tion was still detected in detergent-treated infected cell lysates.IMPORTANCE The entry of enveloped

205 ted T cells and that clonal expansion of HIV-infected cells maintains viral persistence.

206 ed to bind MHC or experimentally eluted from infected cells, making this the most comprehensive datas

207 nisms involving compromised viral sensing in infected cells may thus be central to the described immu

208 ected CCR6+ T cells accounted for nearly all infected cells (median, 89.7%).

209 For replication in infected cells, members of the Reoviridae family form in

210 ression that could otherwise eliminate virus-infected cells; modulating the epigenetic state of the v

211 However, in HCV-infected cells, Mov10 localizes in circular structures s

212 In infected cells, NucC activation leads to complete destru

213 significantly check clonal proliferation of infected cells or greatly alter the provirus landscape i

214 ding to novel approaches to destroy latently infected cells or inhibit reactivation from latency.

215 ) and heterogeneous objects in an Adenovirus-infected cell over large fields of view (1.14 x 1.14 mum

216 Compared to non-infected cells, P. gingivalis infection decreased TEER (

217 bstantial reduction in the proportion of HIV-infected cells per year on therapy within the LN.

218 We show here that expansion of the infected cell population, observed in LECs, but not in b

219 easuring the total or average activity of an infected cell population, which often consists of a mixt

220 tion, alpha-synuclein aggregates appeared in infected cell populations connected to the olfactory bul

221 g a population structure of multiple clones (infected cell populations with identical genomic provira

222 We found that rotavirus-infected cells produce paracrine signals that manifested

223 SIONThese findings show that clones of HIV-1-infected cells producing virus can cause failure of ART

224 read (de novo infection) and mitotic spread (infected cell proliferation), creating a population stru

225 rine receptors having opposing roles in KSHV-infected cell proliferation.

226 imed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN

227 n unit 1 (IEtu1) promoter that drives bovine infected cell protein 0 (bICP0) and bICP4 expression.

228 transcriptional regulatory proteins, bovine infected cell protein 0 (bICP0) and bICP4.

229 scription unit 1 (IEtu1) promoter, the HSV-1 infected cell protein 0 (ICP0) promoter, and the mouse m

230 Infected cell protein 0 (ICP0), an E3 ubiquitin ligase o

231 al phenotyping using CyTOF to trace latently infected cells reactivated ex vivo to their original pre

232 ever, the source of the proliferation of HIV-infected cells remains unclear.

233 on is the main barrier to cure, and most HIV-infected cells reside in the gut, where distinct but unk

234 Most HIV-infected cells reside in tissues such as the gut, but it

235 only some cells in a population of latently infected cells respond to lytic triggers, resulting in s

236 Persistence of EBV-infected cells results in severe lymphoproliferative dis

237 Cryosections of infected cells revealed numerous membranous vesicles ins

238 ndings establish a mechanistic link by which infected cells sense environmental cues to regulate late

239 Accordingly, TBC1D5 depletion from infected cells significantly affected CCV development.

240 how HCMV controls the microenvironment of an infected cell so as to favor productive replication is o

241 hree MPs of Potato virus X (PVX), and in PVX-infected cells, suggesting that reticulon-like MPs are e

242 as prominent near infected cells, but not in infected cells, supporting the hypothesis that bystander

243 IF receptor to areas of E2 expression on the infected cell surface, and LIF enhanced the antiviral ef

244 showed accumulation of Abeta42 mainly in non-infected cells surrounding HSV-1-infected cells.

245 Infected cells synthesized eBD2 and -3, promoting furthe

246 2 [0.035-0.074] days(-1) corresponding to an infected cell t(1/2) = 13.3 days.

247 more permissive to infection by contact with infected cells than by cell-free virus.

248 rocarbon receptor (AhR) in LXA4-treated KSHV-infected cells than in untreated KSHV-infected cells, wh

249 re efficiently and produces higher yields in infected cells than T3D.

250 everal different tegument proteins formed in infected cells that bind to gE/gI and US9.

251 erapy (ART) owing to a reservoir of latently infected cells that contain replication-competent virus(

252 lex pattern of Arf activation in enterovirus-infected cells that may contribute to the resilience of

253 the potential locations of reservoirs of HIV-infected cells that persist during therapy.

254 usceptibility to various degrees in latently infected cells that respond to mechanistically distinct

255 ressed at the surface of viral particles and infected cells that samples different conformations.

256 Superresolution microscopy revealed in infected cells the vertical displacement of paxillin and

257 are obtained for the survival function of an infected cell, the number of bacteria released as a func

258 In infected cells, the CoV RNA-synthesizing machinery assoc

259 Infected cells then turn into new differentiated bacteri

260 ve to inhibition of GBF1, suggesting that in infected cells they do not actively cycle between GTP- a

261 ibited type I interferon (IFN) expression in infected cells through a previously described mechanism,

262 tance capable of destroying tumors and virus-infected cells through cytotoxicity and rapid cytokine p

263 nal capacity to accelerate the loss of virus-infected cells through Fc gamma receptor (FcgammaR)-medi

264 Bluetongue virus (BTV) forms VIBs in infected cells through nonstructural protein 2 (NS2), a

265 us virions by tracking viral cores in living infected cells through viral DNA integration and provira

266 oliferation counterbalanced the decay of HIV-infected cells throughout therapy.

267 ch accumulates at nucleoli of transfected or infected cells, thus perturbing the nuclear import of tr

268 associated with secretory pathways within an infected cell to facilitate efficient viral replication.

269 V-1 Env State 2A has been shown to sensitize infected cells to ADCC.

270 cells to activation sites, causing latently infected cells to compete for survival.

271 ein U (Vpu) promotes viral egress and allows infected cells to evade host immunity.

272 The ability of supernatant from infected cells to induce amylin or Abeta42 aggregation w

273 eptor expression to promote dissemination of infected cells to lymphoid follicles.

274 nowledge regarding mechanisms that allow HIV-infected cells to persist in individuals during combinat

275 On the basis of immunofluorescence, infected cell types included CD68(+) type A (macrophage-

276 LIN sets if the infected cell undergoes superinfection, then the lysis i

277 NK cells provide a defense against virally infected cells using a variety of cytotoxic mechanisms,

278 sed ion-beam scanning electron microscopy of infected cells validated numerous membranous structures

279 peptides previously identified from virally infected cells via mass spectrometry.

280 In the wild-type HVT-infected cells, vNr-13 expression appeared to be directl

281 y, we found that restoration of MHC-I in HIV-infected cells was accompanied by enhanced CTL-mediated

282 Elimination of infected cells was further quantified using a modified f

283 originally thought that the pool of latently infected cells was largely composed of cells harboring t

284 Notably, miR-125b down-regulation in infected cells was not due to reduced pri-miRNA or pre-m

285 The NE gene expression observed in KSHV-infected cells was recapitulated in uninfected endotheli

286 In both human and bovine RSV-infected cells, we demonstrated that the p65 subunit of

287 HVT-infected cells were reported to be relatively more resis

288 tified LXA4-interacting host factors in KSHV-infected cells, which could help provide an understandin

289 d KSHV-infected cells than in untreated KSHV-infected cells, which probably facilitates the affinity

290 progression but does not eliminate latently infected cells, which resupply active virus, thus necess

291 Treatment of SINV-Broccoli-infected cells with antibody to the SINV E2 glycoprotein

292 Treatment of HAZV-infected cells with brefeldin A (BFA), an inhibitor of A

293 Treatment of KSHV-infected cells with LXA4 minimizes the activation of inf

294 NA replication.IMPORTANCE Treatment of HSV-1-infected cells with SP-2509 blocked viral DNA replicatio

295 ncrease in flavivirus infection of Wolbachia-infected cells with the addition of acyl-carnitines.

296 best to measure the numbers of persistently infected cells with the potential to cause viral rebound

297 Treatment of EBV-infected cells with type I interferon inhibits reactivat

298 that HIV RNA is shed due to proliferation of infected cells with virion production.

299 smaller reduction in the proportion of HIV-1-infected cells within LNs per year on therapy that was s

300 ly identify the KSHV replication stage in an infected cell would not only allow us to effectively iso