ライフサイエンスコーパス: virus-infected cell

1 RNA and co-purifies with self-RNA even from virus infected cells.

2 er critical host defense mechanisms removing virus-infected cells.

3 id CD8(+) T cell activation and clearance of virus-infected cells.

4 netheless crucial for the rapid clearance of virus-infected cells.

5 utic strategies and the ability to eradicate virus-infected cells.

6 er siRNA, miRNA, and ribozymes to cancer and virus-infected cells.

7 lectively eliminates dangerous cells such as virus-infected cells.

8 s CD160 on effector NK cells challenged with virus-infected cells.

9 ate innate immune responses toward tumor and virus-infected cells.

10 +) T cells in the skin did not interact with virus-infected cells.

11 has never been conclusively demonstrated in virus-infected cells.

12 at is initiated prior to direct contact with virus-infected cells.

13 nano-sized vesicles produced by healthy and virus-infected cells.

14 onal folding of hemagglutinin in influenza A virus-infected cells.

15 mpaired IFN-beta induction in PKR-sufficient virus-infected cells.

16 were observed in the nuclei of ac79-knockout virus-infected cells.

17 tion of a 45-kDa N-terminal PABP fragment in virus-infected cells.

18 ee proteins was analyzed at the same time in virus-infected cells.

19 HC avidity and less efficient recognition of virus-infected cells.

20 aching levels similar to those seen in C(ko) virus-infected cells.

21 om the D8L protein in TAP-deficient vaccinia virus-infected cells.

22 cytotoxic responses to human and avian fluA virus-infected cells.

23 ative inflammasome complex with caspase-1 in virus-infected cells.

24 K interacted with UL20, as has been shown in virus-infected cells.

25 ituted by plasmid transfection and in mutant virus-infected cells.

26 threat of cell-cycle arrest or apoptosis of virus-infected cells.

27 eracts and colocalizes with VSV P protein in virus-infected cells.

28 tion in UL96, UL32, or UL96/UL32 dual mutant virus-infected cells.

29 the ability to kill diverse tumor cells and virus-infected cells.

30 ively repress IFN-alpha activation in Sendai virus-infected cells.

31 er extent that of the ICP0 gene in wild-type virus-infected cells.

32 r 2, thereby inhibiting protein synthesis in virus-infected cells.

33 ultifunctional protein, is ISG15 modified in virus-infected cells.

34 tumor effects of BMP signaling in normal and virus-infected cells.

35 primarily detected in neurons near areas of virus-infected cells.

36 irus or may internalize antigen derived from virus-infected cells.

37 infection in the membrane fraction of mutant virus-infected cells.

38 of the host cytokine immune response of the virus-infected cells.

39 ted nanotube formation and viral clusters in virus-infected cells.

40 occurred only through endocytosis in Sindbis virus-infected cells.

41 nt L also inhibited viral gene expression in virus-infected cells.

42 d from a subgenomic mRNA in the cytoplasm of virus-infected cells.

43 C(ko)-infected compared to V(ko) or parental virus-infected cells.

44 levels of CCL2 compared to mock- or E3 null virus-infected cells.

45 y and specificity in the staining of various virus-infected cells.

46 n host defense, including the elimination of virus-infected cells.

47 omplement-dependent cytotoxicity of vaccinia virus-infected cells.

48 nfection in wild-type-virus- and ICP0 mutant virus-infected cells.

49 kappaB (NF-kappaB) that becomes activated in virus-infected cells.

50 GAPDH mRNA are rapidly degraded in wild-type virus-infected cells.

51 mokines CCL2 and CCL5 than mock- and E3 null virus-infected cells.

52 for the proliferation and transformation of virus-infected cells.

53 responsible for increased FAO and OXPHOS in virus-infected cells.

54 DV-infected cells but not from double mutant virus-infected cells.

55 3 may help to regulate levels of histones in virus-infected cells.

56 s associated with hyper-induction of IFNs in virus-infected cells.

57 which is consistent with data obtained from virus-infected cells.

58 latory components are not clearly defined in virus-infected cells.

59 cells that was similar to that of wild-type virus-infected cells.

60 ment of mononuclear cells to foci containing virus-infected cells.

61 ly compartment compared to that of wild-type virus-infected cells.

62 s, and to a lesser extent in the DeltaU(L)41 virus-infected cells.

63 inflammation, spatially unrelated to foci of virus-infected cells.

64 nuclei but not in the cytoplasm of wild-type virus-infected cells.

65 clear regions of West Nile virus- and dengue virus-infected cells.

66 ed cytotoxic CD8 T lymphocytes (CTL) to kill virus-infected cells.

67 ion of IRF3 and IFN-beta transcription in Ud virus-infected cells.

68 to levels equal to those found in canarypox virus-infected cells.

69 igase Sel10, leading to proliferation of the virus-infected cells.

70 sponse to RNA molecules that are produced in virus-infected cells.

71 ation, thus blocking the immune detection of virus-infected cells.

72 rotein aggregates in the cytoplasm of mutant virus-infected cells.

73 d by double-stranded RNA (dsRNA) produced in virus-infected cells.

74 iation with the ribonucleoprotein complex in virus-infected cells.

75 result in retention of ICP0 as in wild-type virus-infected cells.

76 at LD-associated sites attached to the ER in virus-infected cells.

77 reverse-transcribed in HIV-1 virions and in virus-infected cells.

78 er amounts of beta interferon than wild-type virus-infected cells.

79 irus in treated patients and the location of virus-infected cells.

80 t-virus-infected cells compared to wild-type-virus-infected cells.

81 necroptosis and leads to rapid death of the virus-infected cells.

82 t hemagglutinin (rHA) protein and homologous virus-infected cells.

83 coded by spliced mRNAs could be expressed in virus-infected cells.

84 t defense systems to recognize and eliminate virus-infected cells.

85 d strongly with ADCC-Abs titers against H7N9 virus-infected cells.

86 ild-type virus-infected cells and the mutant virus-infected cells.

87 deficient in locating, engaging, and killing virus-infected cells.

88 s with elevated Env levels on the surface of virus-infected cells.

89 cell-mediated elimination of transformed and virus-infected cells.

90 infected cells compared to those in parental virus-infected cells.

91 LC3 redistribution to the plasma membrane in virus-infected cells.

92 This novel inhibitor triggers apoptosis of virus-infected cells.

93 d protein (N protein) interacts with RdRp in virus-infected cells.

94 rization of specialized structures formed in virus-infected cells.

95 , and changes in the spatial architecture of virus-infected cells.

96 RF12 activates ERK and inhibits apoptosis in virus-infected cells.

97 assembles and buds at the plasma membrane of virus-infected cells.

98 n expressed on the cell surface of influenza-virus-infected cells.

99 of a PLpro inhibitor blocked deISGylation in virus-infected cells.

100 d facilitates immune-mediated destruction of virus-infected cells.

101 terferon, the antiviral cytokine secreted by virus-infected cells.

102 rus replication complexes in WNV- and dengue virus-infected cells (21).

103 ee system in which mitochondria derived from virus-infected cells activate IRF3 in the cytosol.

104 /CD155 (DNAM-1 ligand), are often induced on virus-infected cells, although some viruses, including h

105 n essential contribution to the clearance of virus infected cells and the resolution of pulmonary inf

106 rmed MHC class I:peptide complexes between a virus-infected cell and an uninfected APC, termed cross-

107 lex containing Cav-1 with M, NP, and HN from virus-infected cells and a complex containing Cav-1 and

108 stent infection by enhancing the survival of virus-infected cells and blocking target cell destructio

109 L-17 augments virus clearance by eliminating virus-infected cells and boosting lytic function by cyto

110 results from T cell-mediated destruction of virus-infected cells and by release of cytokines and che

111 ) use perforin and granzyme B (gzmB) to kill virus-infected cells and cancer cells.

112 Th17 loss correlated with greater levels of virus-infected cells and cell death.

113 y activated T cells for immediate control of virus-infected cells and central memory CD8(+) T cells t

114 in mock-infected or in DeltaVHS RNase mutant-virus-infected cells and does not by itself support the

115 oss-presented influenza antigen derived from virus-infected cells and from free virus particles.

116 PB2-S1 was detected in virus-infected cells and in cells transfected with a pro

117 p38, and NFkappaB-p65 form a signalosome in virus-infected cells and influence downstream expression

118 there are antibodies that bind to influenza virus-infected cells and mediate lysis of the infected c

119 ergoes phosphorylation-induced activation in virus-infected cells and plays an important role in the

120 hy infants, children and adults against H7N9 virus-infected cells and recombinant hemagglutinin (HA),

121 3 mutant-virus-infected but not in wild-type-virus-infected cells and reduced the accumulation of spe

122 e in B cell survival mechanisms is unique to virus-infected cells and relies on regulation of MCL-1 m

123 y (ADCC) Abs by NK cells leads to killing of virus-infected cells and secretion of antiviral cytokine

124 red for the Epo-independent growth of Friend virus-infected cells and that the activation of Stat3 by

125 osphoproteomic profile between the wild-type virus-infected cells and the mutant virus-infected cells

126 of tissue-localized CD8(+) T cells to locate virus-infected cells and thereby exert anti-viral effect

127 itro experiments with human immunodeficiency virus-infected cells and through atomic force microscopy

128 d immunohistochemistry were used to identify virus-infected cells and to determine the numbers and ty

129 Cytotoxic T cells kill virus-infected cells and tumor cells by releasing lytic

130 Cytotoxic T lymphocytes (CTLs) kill virus-infected cells and tumor cells, and play a critica

131 ymphocytes is the key mechanism to eliminate virus-infected cells and tumor cells.

132 ivity is essential in CD8+ T-cell killing of virus-infected cells and tumor cells.

133 cytotoxic lymphocytes to induce apoptosis in virus-infected cells and tumor cells.

134 tein is insufficient to explain its roles in virus-infected cells and tumors.

135 in CTLs and NK cell-mediated elimination of virus-infected cells and tumors.

136 membranes prepared from KPNA4-16 recombinant virus-infected cells and was also detected in microsomes

137 h antibody binding to Env on the surfaces of virus-infected cells and with viral neutralization; howe

138 rotein (found on the surface of both HIV and virus-infected cells) and anti-2,4-dinitrophenyl antibod

139 ire direct antigen-MHC interactions to clear virus-infected cells, and (iii) persistent interactions

140 l spread in mouse lungs, for live imaging of virus-infected cells, and for differential gene expressi

141 unts of shed GP in the medium, GP present in virus-infected cells, and GP present on virions.

142 cleus is severely compromised in UL92 mutant virus-infected cells, and mature virions are not observe

143 resulted in a 60 to 80% reduction in dengue virus-infected cells, and pretreatment of endothelial ce

144 Once in the brain, both free virus and virus-infected cells are able to infect neighboring resi

145 ly studied for many years, the rate at which virus-infected cells are killed in vivo by the CTL respo

146 ecular mechanisms whereby NK cells recognize virus-infected cells are known.

147 roducts of the initial cleavage of wild-type virus-infected cells are themselves subject to proteasom

148 ector and regulatory mechanisms to eliminate virus infected cells as well as fine tune the control of

149 is expressed to normal levels in the mutant virus-infected cells, as are the RNAs for two other prot

150 8+ T cells recognize simian immunodeficiency virus-infected cells at 2 h postinfection, whereas Env-s

151 esponses that can clear the nidus of initial virus-infected cells at mucosal surfaces to prevent muco

152 However, E1B-55K mutant virus-infected cells became trapped in a mitotic-like st

153 and US3-PK, an indication that in wild-type virus-infected cells both proteins are actively stabiliz

154 robust preferential expansion in response to virus-infected cells (both HCMV and influenza) in an ant

155 d to colocalize with RNA Pol II in wild-type-virus-infected cells but not in DeltaU(L)13-infected cel

156 ty (ADCC), the killing of an antibody-coated virus-infected cell by cytotoxic effector cells.

157 ession library, and apoptosis was induced in virus-infected cells by 2,3-dimethoxy-1,4-naphthoquinone

158 Current methods for measuring the killing of virus-infected cells by antibody-dependent cell-mediated

159 tibodies, such as their ability to eliminate virus-infected cells by antibody-dependent cell-mediated

160 an assay designed to measure the killing of virus-infected cells by antibody-dependent cell-mediated

161 Destruction of virus-infected cells by CTL is an extremely sensitive an

162 Elimination of virus-infected cells by cytotoxic lymphocytes is trigger

163 Cytolytic granules mediate killing of virus-infected cells by cytotoxic T lymphocytes.

164 T cells might be directed toward virus-infected cells by expressing HBV-specific receptor

165 resolution analysis of the surface of M-null virus-infected cells by field emission scanning electron

166 This mutation reduces recognition of virus-infected cells by HLA-B*57:03-KF11 CTLs and is ass

167 host innate immune response and apoptosis in virus-infected cells by mediating IRF-3 activation throu

168 elevated viral gene expression in rPIV5-CPI- virus-infected cells can be attributed to a P protein wi

169 Moreover, EVs generated by virus-infected cells can incorporate viral proteins and

170 ither internalized HCMV virions nor THY-1 in virus-infected cells colocalized with transferrin as det

171 a steepened transcription gradient in C(KO) virus-infected cells compared to those in parental virus

172 were found by electron microscopy in mutant-virus-infected cells compared to wild-type-virus-infecte

173 gnificantly higher cytotoxicity against fluA virus-infected cells compared with their CD56(-) counter

174 When the virus-infected cells contained elevated dUTP levels, rev

175 s indicated that IRF-3-mediated apoptosis of virus-infected cells could be an effective antiviral mec

176 tory activity was observed with a variety of virus-infected cell cultures.

177 ability of natural killer (NK) cells to kill virus-infected cells depends on the presence of ligands

178 Neuronal differentiation of control virus-infected cells did not occur at a detectable level

179 how that the presence of immunoreactivity in virus-infected cells does indeed correlate with the abil

180 CD8(+) T cells rapidly recognize virus-infected cells due to the generation of antigenic

181 text of viral particles or on the surface of virus-infected cells, due to enhanced binding of antibod

182 Elimination of influenza virus-infected cells during primary influenza virus infe

183 ors 4GI and 4GII (eIF4GI and eIF4GII) within virus-infected cells, effectively halting cap-dependent

184 functional, antigen-specific T cells, a few virus-infected cells escaped immune clearance and progre

185 NK cells in the elimination of tumor and of virus-infected cells, evidence for a regulatory role for

186 Ectromelia virus-infected cells expressing the major histocompatibi

187 y to visualize immune cell interactions with virus-infected cells following epicutaneous vaccinia vir

188 killer (NK) lymphocytes are known to target virus-infected cells for destruction, their importance i

189 llular retention of the DRs, thus protecting virus infected cells from TRAIL and TRAIL-dependent NK c

190 tion of virus titers, presumably by clearing virus-infected cells from airway mucosa.

191 ally promote viral persistence by protecting virus-infected cells from apoptosis and CD8(+) T cell-me

192 Human influenza A and B viruses infected cells from geographically and evolution

193 te between the RNA content of healthy versus virus-infected cells, functioning as accurate sensors of

194 Mutant virus-infected cells had significantly higher levels of

195 that extracellular vesicles produced by SFTS virus-infected cells harbor infectious virions.

196 n centers in both OriR-transfected cells and virus-infected cells, highlighting a direct involvement

197 ategies that work to regulate translation in virus-infected cells, highlighting both virus-specific t

198 active oxygen species (ROS) are generated by virus-infected cells; however, the physiological importa

199 ion to proviral load and the survival of the virus-infected cell in the host.

200 iderable amounts of surface GP are shed from virus-infected cells in a soluble truncated form by tumo

201 may affect NK cell recognition of influenza virus-infected cells in addition to virus binding to hos

202 ble increase in titers of ADCC-Abs to rHA or virus-infected cells in adults and children who received

203 lity that accumulating CD4 at the surface of virus-infected cells in EC could interact with Env and t

204 easurements and predict CTL efficacy against virus-infected cells in pathogenesis and vaccine studies

205 Immunohistochemistry revealed disseminated virus-infected cells in the junction between the anterio

206 sive PD-1 pathway and suggest a new role for virus-infected cells in the local corruption of immune r

207 bserved in the extracellular space in mutant virus-infected cells in the presence or absence of the D

208 rganization of immune cells interacting with virus-infected cells in tissues remains uncertain.

209 these differences affect CTL recognition of virus-infected cells in vitro.

210 es demonstrate that cytotoxic ICs can target virus-infected cells in vivo but also highlight potentia

211 From the turnover of virus-infected cells in vivo, to rates of thymic product

212 Innate immune recognition of virus-infected cells includes NK cell detection of chang

213 on levels in mock-infected, IFN-treated, and virus-infected cells indicated that WNV infection suppre

214 re specifically reduced by the inhibitors in virus-infected cells, indicating that NF-kappaB signalin

215 hibited IFN-mediated STAT1 activation within virus-infected cells, indicating that RV encodes inhibit

216 formation and decrease the antigenic load of virus-infected cells, indicating that the BHRF1 miRNA cl

217 virus or their exposure to supernatant from virus-infected cells induced the same changes in TLR and

218 on 1 antibodies synergize for recognition of virus-infected cells, infectious virion capture, virus n

219 l disease, including regulating the entry of virus-infected cells into the CNS.

220 al killer (NK) cell recognition of influenza virus-infected cells involves hemagglutinin (HA) binding

221 In RNA-virus infected cells, IRF-3's transcriptional activation

222 CD8(+) T cell recognition of virus-infected cells is characteristically restricted by

223 of ICP4 at the promoters of E and L genes in virus-infected cells is crucial for the formation of tra

224 y of cytotoxic T lymphocytes (CTLs) to clear virus-infected cells is dependent on the presentation of

225 Secretion of interferon (IFN) by virus-infected cells is essential for activating autocri

226 production and the ability of a cell to lyse virus-infected cells is not clear.

227 RIG-I activation and interferon induction in virus-infected cells is not known.

228 ores became depleted in wild-type and mutant virus-infected cells late in infection but increased sig

229 on the host cell, we tested varicella zoster virus-infected cell lysates and clinically isolated viru

230 Western blot analysis of virus-infected cell lysates revealed a significant incre

231 Sindbis virus-infected cells make two positive-strand RNAs, a ge

232 g these, NKp30 is a major receptor targeting virus-infected cells, malignantly transformed cells, and

233 In virus-infected cells MAVS forms prion-like aggregates to

234 Although direct NK-cell-mediated lysis of virus-infected cells may contribute to antiviral defence

235 iosynthetic processes, while in ICP34.5-null virus-infected cells, mostly antiviral genes were up-reg

236 ith a mutant lacking the RNase, in wild-type virus-infected cells mRNA of housekeeping genes exemplif

237 f transcription (Tat), a protein released by virus-infected cells, on synapses between hippocampal ne

238 ficulty in purifying the protein produced in virus-infected cells or by recombinant techniques.

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

240 Further, ICP34.5-null virus-infected cells produced greater amounts of beta in

241 The ac79-knockout virus-infected cells produced plaques smaller than those

242 The immediately early protein of the virus, infected cell protein 0 (ICP0), plays a central r

243 onstruction of deconvolved z-stack images of virus-infected cells provided detailed insight into the

244 s (L-particles) secreted from herpes simplex virus-infected cells provided the first evidence of micr

245 c assay histochemically visualized influenza virus-infected cells regardless of viral hosts and subty

246 13 in vivo (ovo) revealed that the dnBMPR-1B-virus-infected cells remained in the endocardial epithel

247 antiviral therapy, a persistent reservoir of virus-infected cells remains.

248 In influenza A virus-infected cells, replication and transcription of t

249 In hepatitis C virus-infected cells, replication is generally considere

250 showed that hnRNP K suppresses apoptosis of virus-infected cells, resulting in increased cell surviv

251 Super-resolution imaging of virus-infected cells revealed rod-shaped MAVS clusters o

252 assays and in situ hybridization analysis of virus-infected cells revealed that the mutant ts1249 was

253 ized receptors that regulate antigenicity of virus-infected cells reveals determinants of antiviral i

254 Virus-infected cells showed normal development of indivi

255 Ultrastructural examination of virus-infected cells showed that both UL20- and UL11-nul

256 The analysis of protein synthesis in virus-infected cells showed that, at the nonpermissive t

257 In contrast, wild-type virus-infected cells showed the typical spherical, 145-n

258 In the G121E mutant virus-infected cells, STAT1 was not phosphorylated and w

259 presumably due to soluble factors present in virus-infected cell supernatant preparations.

260 These results suggest that B virus-infected cell surfaces maintain normal levels of M

261 activated cell sorter-based screen to select virus-infected cells that nevertheless expressed newly s

262 otein that creates a cellular environment in virus-infected cells that permits productive virus infec

263 We previously demonstrated in measles virus-infected cells that PKR is required for the maxima

264 the remarkable ability of CTL to respond to virus-infected cells that present few cognate pMHC-I com

265 that IFN responses were primarily induced by virus-infected cells that stimulated pDC in a TLR-depend

266 toplasmic inclusion developed in UL32 mutant virus-infected cells that was similar to that of wild-ty

267 t a novel and distinct activity of IRF-3, in virus-infected cells, that induces apoptosis.

268 wo positive-strand mRNAs are made in Sindbis virus-infected cells, the genomic (G) RNA and the subgen

269 Specifically, in wild-type virus-infected cells, the majority of changed genes were

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

271 In both transfection assays and virus-infected cells, the NS1B protein binds and relocal

272 ost cellular translation machinery occurs in virus-infected cells, the role of such alteration and th

273 of an in vitro-generated marked sgmRNA into virus-infected cells, the sgmRNA, like the genome, can f

274 We report that in wild-type virus-infected cells there was a rapid increase in the n

275 way to downregulate HLA class I molecules in virus-infected cells, thereby evading elimination by cyt

276 es constitute only a small percentage of all virus-infected cells, they may be relatively resistant t

277 CD8(+) CTLs detect virus-infected cells through recognition of virus-derive

278 activation of these kinases was sustained in virus-infected cells throughout infection, UV-inactivate

279 ion with specific ligands expressed on tumor/virus-infected cells, thus contributing to immune escape

280 t is recognized by cellular TLR3 and used by virus-infected cells to activate specific transcription

281 the translation machinery upon activation in virus-infected cells to create hurdles for the manufactu

282 3a (ORF3a) and ORF7a-have been identified in virus-infected cells to date.

283 IE transcripts in both wild-type and mutant virus-infected cells to equivalent levels.

284 arget cells and halt virus transmission from virus-infected cells to non-infected cells, thereby prev

285 osomes extracted from cytoplasm of wild-type virus-infected cells treated with CHX and displayed in s

286 rements of nucleocapsid transport in Marburg virus-infected cells under biosafety level 4 conditions.

287 evels of EBOV GP expressed at the surface of virus-infected cells via GP shedding plays an important

288 resented the dominant mechanism by which the virus-infected cell was thought to undergo programmed ce

289 f ILTV gB and gD proteins in the recombinant virus-infected cells was detected by immunofluorescence

290 binant viral vectors, respectively, in which virus-infected cells were detected by flow cytometry of

291 High titers of ADCC-Abs against H7N9 virus-infected cells were detected in sera from adults a

292 In control IgG-treated mice, virus-infected cells were observed only within the AC.

293 isolated from NSs-expressing cells and SFTS virus-infected cells were positive for the viral protein

294 hibited resistance to fusing with A56 mutant virus-infected cells, whereas expression of A56 or K2 al

295 gglutinin is localized within lipid rafts in virus-infected cells, whereas M2 is associated at the pe

296 al simulations that our system can eliminate virus-infected cells, which are characterized by a tende

297 Treatment of CX3C virus-infected cells with the F(ab')2 form of an anti-G

298 Remarkably, after treating virus-infected cells with the RNA splicing inhibitor spl

299 heral virus replication, yet how they locate virus-infected cells within tissues is unknown.

300 class I presented epitopes on the surface of virus infected cells, yet the number and origin of the v