ライフサイエンスコーパス: latently

1 , and what have been previously described as latently activated Entner-Doudoroff and glyoxylate shunt

2 mics of HIV-1 mRNA and protein expression in latently and newly infected cells on the single-cell lev

3 Latently EBV-infected epithelial cells, as well as other

4 Here, we demonstrate that latently expressed HCMV miR-US5-2 downregulates the tran

5 Our data suggest that latently expressed viral miRNAs manipulate stem cell hom

6 HIV can actively infect and/or can persist latently for years by manipulating host epigenetics; how

7 To understand the persistence of latently HIV-1 infected cells in virally suppressed infe

8 nresponsive, anergy-like T cell phenotype of latently HIV-1 infected host cells.

9 ndicates transcriptional differences between latently HIV-1 infected T-cells and macrophages and prov

10 The same combination eliminated reactivated latently HIV-1-infected cells in an ex vivo quantitative

11 that inhibition of Naf1 activity to activate latently HIV-1-infected cells may be a potential therape

12 Following stimulation of latently HIV-1-infected J89 cells with human tumor necro

13 ficantly enhanced viral reactivation in both latently HIV-1-infected Jurkat T cells and primary centr

14 The low frequency of latently HIV-infected cells in vivo limits the testing o

15 The persistence of latently HIV-infected cellular reservoirs represents the

16 lated and recruited into the mitochondria in latently HIV-infected macrophages both in vitro and in v

17 One of these reservoirs are latently HIV-infected macrophages.

18 n reducing the rate of HSV-1 reactivation in latently HSV-1-infected IFN-gamma-KO mice.

19 oral glutamine reduced virus reactivation in latently HSV-1-infected mice and HSV-2-infected guinea p

20 criptome analysis of trigeminal ganglia from latently HSV-1-infected, glutamine-treated WT mice showe

21 r at sequences of homology with EBV, present latently in B cells, which may be coinfected with both v

22 Human cytomegalovirus (HCMV) resides latently in hematopoietic progenitor cells (HPCs).

23 that reactivation of HIV-1 expression in the latently infected ACH-2 cell line elicited antibody-medi

24 e enabled the phenotypic characterization of latently infected and de novo-infected cells dependent o

25 anglia (TG) and the brain stem from the same latently infected animal using direct assays of equivale

26 owever, this hypothesis remained untested in latently infected animals.

27 anipulation of EBV BHRF1-2 miRNA activity in latently infected B cells altered steady-state cytokine

28 TANCE The EBV protein EBNA3A is expressed in latently infected B cells and is important for efficient

29 As indicated by coimmunoprecipitation, in latently infected B cells that are stimulated to reactiv

30 tibody positivity, high loads of circulating latently infected B cells, and a marked lymphocytosis ca

31 Here we demonstrate that in latently infected B cells, EBER1 transcripts interact wi

32 Our results show that latently infected B lymphoma cells demonstrated signific

33 the antiproliferative effect of IFN-alpha on latently infected BL cells.

34 n a subset of trigeminal ganglion neurons in latently infected calves but not in uninfected calves.

35 Latently infected calves consistently reactivate from la

36 ly more neurons in the trigeminal ganglia of latently infected calves than in those of uninfected cal

37 ons is not detectable following treatment of latently infected calves with the synthetic corticostero

38 detected in beta-catenin-positive neurons in latently infected calves.

39 Following ex vivo activation of latently infected CD4 T cells without de novo infection,

40 HIV persists in latently infected CD4(+) T cells during antiretroviral t

41 very short time frame to eliminate residual latently infected CD4(+) T cells that become reactivated

42 (CAR) T cells have been developed to target latently infected CD4(+) T cells that express virus eith

43 lves the induction of HIV-1 transcription in latently infected CD4(+) T cells with the goal of elimin

44 induction of transcription of HIV-1 genes in latently infected CD4(+) T cells, followed by the elimin

45 been thwarted by the persistent reservoir of latently infected CD4(+) T cells, which reinitiate syste

46 have focused primarily on the elimination of latently infected CD4(+) T cells.

47 The existence of long-lived reservoirs of latently infected CD4+ T cells is the major barrier to c

48 ocused on developing strategies to eliminate latently infected CD4+ T cells, which represent the majo

49 HIV-1 can remain transcriptionally silent in latently infected CD4+ T cells.

50 a driving force for stabilizing the pool of latently infected CD4+ T cells.

51 rvoir by stimulating the clonal expansion of latently infected CD4+ T cells.

52 etectable levels, although virus persists in latently infected CD4+ T cells.

53 This strategy was also used in a latently infected CD4+ T-cell model after treatment with

54 otoxic effector cells to eliminate the HIV-1 latently infected CD4+ T-cell reservoir.

55 However, not every latently infected cell exposed to a lytic trigger turns

56 Overexpression of A3A in latently infected cell lines led to lower reactivation,

57 e the fraction of reactivatable virus in the latently infected cell population that establishes in vi

58 hat the expression of US28 on the surface of latently infected cells allows monocytes and their proge

59 Strategies that target these latently infected cells and allow immune recognition and

60 llular metabolic pathways can both eliminate latently infected cells and block lytic replication, the

61 establishment and persistence of the pool of latently infected cells and review the current approache

62 ategy aims to reactivate HIV-1 expression in latently infected cells and subsequently eliminate the r

63 ill," aims to reactivate HIV-1 expression in latently infected cells and subsequently eliminate the r

64 this persisting reservoir by reactivation of latently infected cells are currently being developed an

65 ch complicated by knowledge deficits for how latently infected cells are established, maintained, and

66 r factors that facilitate HIV replication in latently infected cells are known.

67 sviruses, however, a substantial fraction of latently infected cells are resistant to lytic-phase-ind

68 Our previous findings showed that latently infected cells are sensitive to inhibitors of c

69 sal and immune-mediated elimination of these latently infected cells are some of the goals of current

70 nuclear antigen (LANA) protein functions in latently infected cells as an essential participant in K

71 Epstein-Barr virus (EBV) genomes persist in latently infected cells as extrachromosomal episomes tha

72 crochips can be potentially used for sorting latently infected cells based on their electrical proper

73 is of a therapeutic strategy for eliminating latently infected cells before haematopoietic stem cell

74 nd experiments, we suggest that the death of latently infected cells brought about by pyroptosis, or

75 As expected, this specific targeting of latently infected cells by F49A-FTP also robustly reduce

76 Superinfection of latently infected cells by productive virus could simila

77 In this study, we show that latently infected cells can proliferate in response to m

78 As latently infected cells cannot be phenotyped directly, t

79 suppressed subjects, the approach identified latently infected cells capable of producing HIV mRNA an

80 on is prevented by a persistent reservoir of latently infected cells capable of reinitiating systemic

81 Latently infected cells carry a circularized EBV episome

82 equently, for transplant recipients, killing latently infected cells could have far-reaching clinical

83 nd contribute to the long-lived reservoir of latently infected cells during antiretroviral therapy (A

84 HIV-1 establishes a pool of latently infected cells early following infection.

85 cells and potentially enable elimination of latently infected cells from the host.

86 Distinguishing and separating live, latently infected cells from uninfected cells is not eas

87 10-1074 treatment depletes the reservoir of latently infected cells harboring replication competent

88 studies indicate that proliferation of these latently infected cells helps maintain the HIV-1 reservo

89 revious studies have quantified this pool of latently infected cells in Americans; however, no study

90 However, the small numbers of latently infected cells in individuals treated during hy

91 ncy that recapitulate the characteristics of latently infected cells in vivo is crucial to identifyin

92 that may better recapitulate the behavior of latently infected cells in vivo This model can be used t

93 s undergoing permissive lytic infections and latently infected cells in which the virus is induced to

94 rategy predicates that virus reactivation in latently infected cells is required to eliminate the hum

95 e potential of ADCC to eliminate reactivated latently infected cells is warranted.

96 the lack of expression of viral antigens on latently infected cells makes them difficult to identify

97 Reactivation of these latently infected cells may result in three fates: 1) ce

98 egies to reduce KSHV episomal persistence in latently infected cells might lead to approaches to prev

99 cy is leading to novel approaches to destroy latently infected cells or inhibit reactivation from lat

100 dimensional phenotyping using CyTOF to trace latently infected cells reactivated ex vivo to their ori

101 equired after curative treatment if residual latently infected cells remain.

102 enomes in only some cells in a population of latently infected cells respond to lytic triggers, resul

103 oviral therapy (ART) owing to a reservoir of latently infected cells that contain replication-compete

104 infection, HIV-1 establishes a reservoir of latently infected cells that persist during antiretrovir

105 virus (HIV-1) eradication is a reservoir of latently infected cells that persists despite long-term

106 e lytic susceptibility to various degrees in latently infected cells that respond to mechanistically

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

108 tes miR-UL148D inhibits ACVR1B expression in latently infected cells to limit proinflammatory cytokin

109 anscription 3) curtail the susceptibility of latently infected cells to lytic cycle activation signal

110 8, lysine 207, and lysine 219) cannot induce latently infected cells to produce and/or release infect

111 the host by intermittently reactivating from latently infected cells to produce viral progenies.

112 ervoir may need to consider the potential of latently infected cells to proliferate.

113 However, a fraction of latently infected cells undergo spontaneous reactivation

114 ed increased lytic reactivation of KSHV from latently infected cells upon STAT3 repression with siRNA

115 e it was originally thought that the pool of latently infected cells was largely composed of cells ha

116 re for HIV is hindered by the persistence of latently infected cells which constitute the viral reser

117 T-cell exhaustion markers may identify those latently infected cells with a higher proclivity to vira

118 represents a possible strategy to eliminate latently infected cells without increasing virion produc

119 kinase pathways p38 and JNK were modified in latently infected cells, and activation of p38 and JNK s

120 ys an inhibitory role in the reactivation of latently infected cells, corroborating its repressive ef

121 f EBER1, a noncoding RNA highly expressed in latently infected cells, in the presence of HPV.

122 ly localized and functions in the nucleus of latently infected cells, playing a pivotal role in the r

123 been shown to trigger HIV transcription from latently infected cells, via a CDK9/HMBA inducible prote

124 after infection, HIV-1 establishes a pool of latently infected cells, which hide from the immune syst

125 s disease progression but does not eliminate latently infected cells, which resupply active virus, th

126 f the very early formation of a reservoir of latently infected cells.

127 ory soluble proteins, or cellular markers of latently infected cells.

128 the long-term persistence of a reservoir of latently infected cells.

129 l receptor (TCR)-induced HIV reactivation in latently infected cells.

130 a requirement for detecting exceedingly rare latently infected cells.

131 uals but does not eliminate the reservoir of latently infected cells.

132 especially important to efforts to eradicate latently infected cells.

133 HIV infection, the in vivo proliferation of latently infected cells.

134 rategies are being investigated to eliminate latently infected cells.

135 racil-rich non-coding RNAs (called HSURs) in latently infected cells.

136 y not be sufficient to eliminate reactivated latently infected cells.

137 d improve the effector functions that target latently infected cells.

138 but are undercut by the inability to target latently infected cells.

139 munity and has been shown to induce HIV from latently infected cells.

140 is persistently maintained in reservoirs of latently infected cells.

141 hondrial genomes leads to increased death in latently infected cells.

142 rebound, attributed to a pool of long-lived, latently infected cells.

143 when MIEP activity is limiting, as occurs in latently infected cells.

144 d the reactivation of silent proviral DNA in latently infected cells.

145 ich act synergistically to reactivate HIV in latently infected cells.

146 ed to reactivate proviral gene expression in latently infected cells.

147 is the difficulty in targeting and measuring latently infected cells.

148 A) mediates persistence of viral episomes in latently infected cells.

149 nent of a multipronged approach to eliminate latently infected cells.

150 and primary isolates) and provirus-activated latently infected cells.

151 ell genes important for enhanced survival of latently infected cells.

152 proinflammatory and antiapoptotic changes in latently infected cells.

153 antly reduced numbers of viral copies in the latently infected cells.

154 response and promotes virus reactivation of latently infected cells.

155 fection because of a persistent reservoir of latently infected cells.

156 unity to interfere with the proliferation of latently infected cells.

157 , depleted the patient-derived population of latently infected cells.

158 o the existence of a long-lived reservoir of latently infected cells.

159 y initiated from in vivo-reactivated primary latently infected cells.

160 plications for strategies toward eliminating latently infected cells.IMPORTANCE The "shock and kill"

161 n the establishment of a stable reservoir of latently infected cells; ART is usually required to keep

162 tion of infectious virus in about 25% of the latently infected cultures.

163 he amount of CXCL10 in trigeminal ganglia of latently infected CXCL10-deficient mice significantly re

164 Strikingly, explant of latently infected dorsal root ganglia revealed a decreas

165 up to 2-fold greater in type III than type I latently infected EBV B cells.

166 tion specifically inhibited the expansion of latently infected endothelial cells and led to increased

167 V, identification of host vulnerabilities in latently infected endothelial cells could be exploited t

168 sential for the survival or proliferation of latently infected endothelial cells in culture, but not

169 ow that Nrf2 activation was elevated in KSHV latently infected endothelial cells independently of oxi

170 ynthesis (FAS) pathways, for the survival of latently infected endothelial cells.

171 We showed that KSHV latently infected epithelial and endothelial cells trans

172 ion was sufficient to induce reactivation in latently infected epithelial cells derived from gastric

173 two approaches for measuring reactivation in latently infected explanted ganglia by sampling media fr

174 euronal axons is vital, allowing spread from latently infected ganglia to epithelial tissues, where v

175 , or the rate of reactivation from explanted latently infected ganglia.

176 -specific IFN-gamma-producing CD8 T cells in latently infected ganglia.

177 vation following murine transplantation of a latently infected graft.

178 nd the sacral sympathetic ganglia (SSG) from latently infected guinea pigs.

179 high)CD8(+) tissue-resident T cells in TG of latently infected HLA-A*0201-transgenic mice and reduced

180 f 24 index tuberculosis (TB) cases and their latently infected household contacts who developed activ

181 A key step during HCMV reactivation in latently infected HPCs is reexpression of viral major im

182 , and the CD8(+)T cells that reside in HSV-1 latently infected human and rabbit trigeminal ganglia (T

183 Using this assay, we found that latently infected human CD4 T cells can be readily detec

184 of integrated HIV-1 proviral DNA copies from latently infected human CD4+ T-cells.

185 We show that knockdown of A3A in latently infected human primary CD4 T cells enhanced HIV

186 peptide was also recognized by T cells from latently infected humans, as evidenced by IFN-gamma rele

187 dCA potently inhibits SIV reactivation from latently infected Hut78 cells and from primary CD4(+) T

188 ted CD8(+) T cell clone isolated from an Mtb latently infected individual as a peptide from the Mtb p

189 It is believed that a small number of latently infected Kaposi sarcoma tumor cells undergo spo

190 ects without HHV-6B plasma detection or from latently infected LCLs.

191 n the majority of suppressed animals contain latently infected M s.

192 bacteria and prevented reactivation of TB in latently infected macaques.

193 tment-mediated clearance of Mtb infection in latently infected macaques.Methods: Sixteen NHPs were in

194 -renewal/proliferation, and proliferation of latently infected memory CD4(+) T cells plays a key role

195 the trigeminal ganglia and the brain stem of latently infected mice following a reactivation stimulus

196 TG explants from the latently infected mice shed significantly higher levels

197 We determined MHV-68-specific CD8 T cells in latently infected mice use either IFN-gamma or perforin/

198 IFN-gamma, and PD-1 transcripts in the TG of latently infected mice.

199 In contrast, addition of LPS directly to latently infected monocytes was not sufficient to trigge

200 ion of both LAT-encoded miRNAs and miR-H6 in latently infected mouse ganglia.

201 We demonstrate HSV-1 reactivation from latently infected mouse neurons induced by forskolin req

202 of ICP0 and other lytic genes in acutely and latently infected mouse trigeminal ganglia.

203 CMV latency, and one viral gene expressed by latently infected myeloid cells is US28.

204 t is well recognized that differentiation of latently infected myeloid progenitor cells to dendritic

205 Furthermore, the latently infected neurons exhibited higher VGSC activity

206 mise, they yield relatively small numbers of latently infected neurons for biochemical and molecular

207 A viral protein (ORF2) expressed in latently infected neurons interacted with beta-catenin a

208 iral protein (ORF2) expressed in a subset of latently infected neurons stabilized beta-catenin and MA

209 Treatment of the latently infected neurons with Ab to NGF resulted in pro

210 an effective means of eliminating HSV-1 from latently infected neurons, efforts to control the virus

211 the frequency and timing of reactivation in latently infected neurons.

212 gesting that these genes enhance survival of latently infected neurons.

213 s of viral replication (rather than becoming latently infected or undergoing cell death) informs the

214 Following transplantation of a latently infected organ, reactivation can occur and cons

215 There is direct evidence that vIL-6 promotes latently infected PEL cell viability and proliferation a

216 oma (PEL) and endothelial cells and sustains latently infected PEL cell viability.

217 ased the production of infectious virus from latently infected primary CD34(+) HPCs.

218 interaction contributes to the viability of latently infected primary effusion lymphoma (PEL) cells

219 igand-induced maturation of iLC derived from latently infected progenitors was not associated with ro

220 -resident HSV-specific CD8(+) T(RM) cells in latently infected rabbits was associated with protection

221 wth assay was used to determine frequency of latently infected rCD4 cells containing replication-comp

222 The median frequency of latently infected rCD4 cells in this Ugandan cohort was

223 Long-lasting, latently infected resting CD4(+) T cells are the greates

224 odeficiency virus type 1 (HIV-1) persists in latently infected resting CD4+ T cells (rCD4 cells), pos

225 ciated with increased proviral expression in latently infected resting cells.

226 heir body fluids following reactivation from latently infected sensory ganglia, the majority never de

227 (BoHV-1) expresses an abundant transcript in latently infected sensory neurons, the latency-related (

228 svirus 1 (BoHV-1) is abundantly expressed in latently infected sensory neurons.

229 T cell proliferation and clonal expansion of latently infected T cells due to viral integration into

230 A long-lived reservoir of latently infected T cells prevents antiretroviral therap

231 These latently infected T cells represent an extremely small p

232 BRD4S was enriched in chromatin fractions of latently infected T cells, and it was more rapidly displ

233 HIV establishes a reservoir in latently infected T cells, and this reservoir has long h

234 cours et al. identifies CD32a as a marker of latently infected T cells, potentially opening the way t

235 ion that induces proviral gene expression in latently infected T cells.

236 ls from several women reactivated HIV-1 from latently infected T cells.

237 l role in preventing virus reactivation from latently infected TG and subsequent virus shedding in te

238 in which HSV-1 reactivation was induced from latently infected TG by UV-B light.

239 at Tim-3 expression on CD8(+) T cells in the latently infected TG is influenced by viral gene express

240 e of exhausted HSV-specific CD8(+)T cells in latently infected TG, thus allowing for increased viral

241 ersistent viral gene expression in the HSV-1 latently infected TG.

242 These results strongly suggest that latently infected tissue M s can reestablish productive

243 aping CD8(+) T cell immunity, locally within latently infected tissues, which protects against recurr

244 e novo KSHV-infected endothelial cells, KSHV latently infected TIVE-LTC and PEL cells, and Kaposi's s

245 This suggests that latently infected TN cells may be a major source of viru

246 Swabbing the corneas of latently infected tree shrews revealed that tree shrews

247 ional CD8(+) TEM and CD8(+) TRM cells within latently infected trigeminal ganglia following virus rea

248 murine model, in which HSV-1 reactivation in latently infected trigeminal ganglia was induced by UV-B

249 ier to an HIV-1 cure is the existence of the latently infected viral reservoir that gives rise to reb

250 T cells in reactivated TG explants from mice latently infected with (i) the avirulent HSV-1 strain RE

251 tion at early times postreactivation in mice latently infected with 17syn+ virus.

252 blocking explant reactivation in TG of mice latently infected with avirulent or virulent HSV-1.

253 gene expression in sensory neurons of calves latently infected with BoHV-1, culminating in virus shed

254 Importantly, we observed that monocytes latently infected with DeltamiR-UL148D are more responsi

255 recognize and respond to autologous B cells latently infected with Epstein-Barr virus (EBV).

256 n latency in trigeminal ganglia (TG) of mice latently infected with herpes simplex virus 1 (HSV-1).

257 CE Approximately 2/3 of adults worldwide are latently infected with herpes simplex virus 1.

258 y, NPC-derived daughter cells appeared to be latently infected with HIV.

259 03 on primary human CD4(+) T cells that were latently infected with HIV.

260 nglion (TG) explants from Swiss Webster mice latently infected with HSV-1, strain McKrae.

261 an be differentiated into mature neurons and latently infected with HSV-1.

262 The persistent reservoir of cells latently infected with human immunodeficiency virus (HIV

263 Quiescence is a hallmark of CD4(+) T cells latently infected with human immunodeficiency virus 1 (H

264 ent study demonstrate that endothelial cells latently infected with KSHV express several neuronal and

265 In B lymphocytes latently infected with KSHV, specific inhibitors of KSHV

266 ., LAT(+)TG) is significantly higher than TG latently infected with LAT-null mutant (i.e., LAT(-)TG).

267 )T cells in the TG of HLA transgenic rabbits latently infected with LAT-null mutant (i.e., LAT(-)TG).

268 [UI] 16.4 million-21.7 million) people were latently infected with MDR tuberculosis in 2014-a global

269 rtality worldwide, as two billion people are latently infected with Mtb.

270 t approximately 1.7 billion individuals were latently infected with Mycobacterium tuberculosis (M.tb)

271 unique TCRbeta sequences from 58 individuals latently infected with Mycobacterium tuberculosis (Mtb)

272 ern and is recognized by T cells from humans latently infected with Mycobacterium tuberculosis By com

273 tage of two well-defined cohorts of subjects latently infected with Mycobacterium tuberculosis or pat

274 of the global population is estimated to be latently infected with Mycobacterium tuberculosis We per

275 Spindle cells are predominantly latently infected with only a small percentage of cells

276 s had a 3-fold lower frequency of rCD4 cells latently infected with replication-competent HIV-1, comp

277 ranscription was markedly reduced in neurons latently infected with VOka compared with POka.

278 The reactivation phenotype of TG that are latently infected with wild-type HSV-1 or with LAT-rescu

279 re found in the TG of HLA transgenic rabbits latently infected with wild-type HSV-1 or with LAT-rescu

280 We then compared reactivation of MHV68 from latently infected WT, Unc93b (-/-), Tlr7 (-/-) Tlr9 (-/-

281 ell death that occurs in a resting (and thus latently infected) T cell when a productively infected c

282 F2-positive trigeminal ganglionic neurons of latently infected, but not mock-infected, calves.

283 TG explants from latently infected, but not uninfected, TG contained sign

284 d pathogen, with 80% of the population being latently infected.

285 e lifelong therapy because of a reservoir of latently-infected cells that harbor replication competen

286 latency- reversing agents (LRAs) could make latently-infected cells vulnerable to clearance by immun

287 onal human adaptive immune responses in HCMV latently-infected huBLT (humanized Bone marrow-Liver-Thy

288 , caused by Mycobacterium tuberculosis (Mtb) latently infects approximately one-fourth of the world's

289 KSHV latently infects cells, and its genome persists as a mul

290 lovirus (HCMV) is a ubiquitous pathogen that latently infects hematopoietic cells and has the ability

291 on-PCR (qRT-PCR) analyses confirm that HSV-1 latently infects neurons of the TG.

292 Epstein-Barr virus (EBV) latently infects normal B cells and contributes to the d

293 nstrate that the CRISPR/Cas9 system disrupts latently integrated viral genome and provides long-term

294 % difference in capture efficiencies between latently KSHV-infected and uninfected BJAB B lymphoma ce

295 e demonstrate that knockdown of IFI16 in the latently KSHV-infected B-lymphoma BCBL-1 and BC-3 cell l

296 Knockdown of Bcr in latently KSHV-infected BCBL-1 cells increased the levels

297 Comparisons of the immune responses of latently M. tuberculosis-infected (LTBI) subjects to tho

298 is was validated in an independent cohort of latently Mtb-infected individuals.

299 o Zp.IMPORTANCE EBV, a human herpesvirus, is latently present in most nasopharyngeal carcinomas, Burk

300 one of nine human herpesviruses that persist latently to establish permanent residence in their hosts