ライフサイエンスコーパス: virus-infected cell

1 s that contributes to the destruction of the virus-infected cell.

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

3 s, possibly through phagocytosis of virus or virus-infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 the capacity of T cells to detect and clear virus-infected cells.

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

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

27 tent antiviral innate immune response in DNA virus-infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 3 may help to regulate levels of histones in virus-infected cells.

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

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

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

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

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

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

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

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

74 receptors (NKR) to distinguish healthy from virus-infected cells.

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

76 -mediated elimination of both free virus and virus-infected cells.

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

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

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

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

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

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

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

84 y innate cytokines and viral ligands to kill virus-infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 K) cells are cytotoxic lymphocytes targeting virus-infected cells and cancer cells.

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

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

106 ulated endoribonuclease that is activated in virus-infected cells and cleaves single-stranded viral a

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

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

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

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

111 tralization or cytotoxic CD8 cell killing of virus-infected cells and may be mediated in part by CD4

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

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

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

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

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

117 MV to effectively block NK cell targeting of virus-infected cells and the major histocompatibility co

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

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

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

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

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

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

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

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

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

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

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

129 efence by tagged mitochondria selectively in virus-infected cells and will be instrumental to identif

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

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

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

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

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

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

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

137 ectrometry for global proteomic profiling of virus-infected cells, and the identification of a candid

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

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

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

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

142 In addition to using native virus infected cells as positive control material, the e

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

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

145 nonneutralizing antibodies (NNAbs) that kill virus-infected cells, as these antibody specificities ha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 PORTANCE High-throughput sequencing (HTS) of virus-infected cells can be used to study in great detai

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

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

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

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

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

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

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

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

173 evidently processed GP1 and GP2 subunits in virus-infected cells, despite the fact that the same mut

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

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

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

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

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

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

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

181 Ectromelia virus-infected cells expressing the major histocompatibi

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

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

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

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

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

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

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

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

190 Mutant virus-infected cells had significantly higher levels of

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

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

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

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

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

196 cts influenza outcomes, recognizes influenza virus-infected cells in a high mannose-dependent manner.

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

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

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

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

201 re scRNAseq can detect DENV RNA and quantify virus-infected cells in physiologically relevant conditi

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

203 and preferentially associated with vaccinia virus-infected cells in the LN paracortex, which led to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 in expression that could otherwise eliminate virus-infected cells; modulating the epigenetic state of

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

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

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

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

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

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

237 Current models fail to explain how virus-infected cells rapidly appear within the LN interi

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

239 In virus-infected cells, RelA typically induces the express

240 13 in vivo (ovo) revealed that the dnBMPR-1B-virus-infected cells remained in the endocardial epithel

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

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

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

244 Papaverine treatment of influenza-virus-infected cells resulted in the inhibition of virus

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

246 ersion of LEF-10 into an aggregated state in virus-infected cells, resulting in the inhibition of vir

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

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

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

250 Virus-infected cells showed normal development of indivi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 In virus-infected cells, the Us11 protein drastically reduc

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

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

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

272 resistance capable of destroying tumors and virus-infected cells through cytotoxicity and rapid cyto

273 dditional capacity to accelerate the loss of virus-infected cells through Fc gamma receptor (FcgammaR

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

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

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

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

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

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

280 llular mechanism that effectively sacrifices virus-infected cells to maintain homeostasis between the

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

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

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

284 Influenza virus-infected cells vary widely in their expression of

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

286 Within influenza virus infected cells, viral genomic RNA are selectively

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

288 the autophagy regulators ULK1 and Beclin1 in virus-infected cells was dependent upon the HSV-1 Us3 Se

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 adhesion of T cells to their targets, e.g., virus-infected cells, which depends on T cell receptor (

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