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 ion lymphoma (PEL) cells, vIL-6 is expressed latently and is essential for normal cell growth and via

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

4 ession of BGLF2 enhanced BZLF1 expression in latently EBV-infected lymphoblastoid cell lines, and kno

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

6 stability is somewhat surprising, since the latently HIV-1 infected CD4(+) memory T cells that form

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

8 sduction and transcription factor network of latently HIV-1 infected host cells are essential to the

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

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

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

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

13 onstrate that the kinase activity profile of latently HIV-1-infected T cells is altered relative to t

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

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

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

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

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

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

20 monly acquired during childhood and persists latently in B cells.

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

22 the ability to infect and transform B cells latently in vitro.

23 d individuals, yet HCMV is carried silently (latently) in 50 to 90% of the population.

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

25 a large overlap in the lesion types found in latently infected and active TB patients.

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

27 y memory CD8(+) T cell pool was decreased in latently infected animals, abrogating the boosting effec

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

29 infection, that they become productively or latently infected at low levels, and that SAMHD1 express

30 re, patient-derived HXTCs were able to clear latently infected autologous resting CD4(+) T cells foll

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

32 is the link between viral reactivation from latently infected B cells and plasma cell differentiatio

33 Latently infected B cells are a major KSHV reservoir, an

34 Thus, 18-5p expression in latently infected B cells has the effect of blocking vir

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

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

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

38 ders, including lymphomas, reactivation from latently infected B lymphocytes occurs upon terminal dif

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

40 is results in a boost of KSHV replication in latently infected B-lymphoma cells.

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

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

43 Latently infected calves consistently reactivate from la

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

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

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

47 llowing allo-HSCT may drive the expansion of latently infected CD27+ B lymphoblasts in the peripheral

48 The ability to persist long term in latently infected CD4 T cells represents a characteristi

49 This is mainly due to the presence of latently infected CD4 T cells, which are not susceptible

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

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

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

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

54 The latent reservoir consisting of latently infected CD4+ T cells represents a major obstac

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

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

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

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

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

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

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

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

63 protein could potentially help to eliminate latently infected cells and deplete the viral reservoir

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

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

66 r, panobinostat did not reduce the number of latently infected cells and this approach may need to be

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

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

69 Because latently infected cells are long-lived, immunologically

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

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

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

73 udescent infection by reactivation from many latently infected cells at multiple sites.

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

75 The model illustrates how the pool of latently infected cells becomes rapidly established duri

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

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

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

79 Superinfection of latently infected cells by productive virus could simila

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

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

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

83 Elimination of latently infected cells could therefore reduce treatment

84 en challenged with type I and II interferon, latently infected cells demonstrated a blockade of signa

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

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

87 ion in most individuals but cannot eradicate latently infected cells established before ART was initi

88 In HIV-1 infection, a population of latently infected cells facilitates viral persistence de

89 However, their effects on latently infected cells from infected individuals remain

90 ach, HDACi have induced HIV RNA synthesis in latently infected cells from some patients.

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

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

93 Because latently infected cells have to undergo viral reactivati

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

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

96 hts into the long-term dynamics of virus and latently infected cells in HIV patients on suppressive t

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

98 othesised that quantification of the pool of latently infected cells in primary HIV-1 infection (PHI)

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

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

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

102 Latently infected cells initiate differentiation to CD19

103 ion, the activation of IE gene expression in latently infected cells is not sufficient to result in p

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

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

106 Blocking the proliferation of latently infected cells might be a good strategy.

107 thesis positing that viruses stored early in latently infected cells preferentially transmit or estab

108 cs of HIV transcription and virus release in latently infected cells reactivated ex vivo.

109 Latently infected cells remain a primary barrier to erad

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

111 Furthermore, knockdown of ISG15 in latently infected cells resulted in a higher level of KS

112 rebound viremia due to reactivation of rare latently infected cells that persist after potentially c

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

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

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

116 ctor STAT3 to regulate the susceptibility of latently infected cells to lytic triggers.

117 pesviruses, is the partial permissiveness of latently infected cells to lytic-cycle-inducing agents.

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

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

120 zation in newly infected cells as well as in latently infected cells undergoing lytic induction and s

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

122 emonstrated to induce HIV transcription from latently infected cells when administered to patients.

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

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

125 Latently infected cells with intermediate transcription

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

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

128 that HDAC6 is expressed diffusely throughout latently infected cells, but its expression level and nu

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

130 that induce active viral gene expression in latently infected cells, followed by immune-mediated kil

131 osi sarcoma-associated herpesvirus (KSHV) in latently infected cells, is required for stable maintena

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

133 IV-1 infection can limit the number of these latently infected cells, raising the possibility that th

134 te viral replication prior to mitosis of the latently infected cells, suggesting that LANA possesses

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

136 g target cells, productively infected cells, latently infected cells, virus, and cytotoxic T lymphocy

137 To characterize these latently infected cells, we studied the integration prof

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

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

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

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

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

143 rategies are being investigated to eliminate latently infected cells.

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

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

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

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

148 proinflammatory and antiapoptotic changes in latently infected cells.

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

150 infected cells to ensure the survival of the latently infected cells.

151 a requirement for detecting exceedingly rare latently infected cells.

152 elusive due to the persistence of long-lived latently infected cells.

153 ual cellular and viral Bcl-2 proteins within latently infected cells.

154 DCML of HIV-1 virions and provirus-activated latently infected cells.

155 ng pathways important for its persistence in latently infected cells.

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

157 both virus replication and reactivation from latently infected cells.

158 tegrate their genomes into host telomeres of latently infected cells.

159 cell population contains both uninfected and latently infected cells.

160 cellular IL-10 and CCL8 in the secretomes of latently infected cells.

161 cycle and the generation and maintenance of latently infected cells.

162 t microenvironment and increased survival of latently infected cells.

163 lytic EBV reactivation when overexpressed in latently infected cells.

164 marker CD2 was expressed at higher levels on latently infected cells.

165 g HIV infection is targeting and eliminating latently infected cells.

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

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

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

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

170 is persistently maintained in reservoirs of latently infected cells.

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

172 especially important to efforts to eradicate latently infected cells.

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

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

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

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

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

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

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

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

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

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

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

184 In latently infected ganglia, HSVs express a long noncoding

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

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

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

188 ed that HCMV IE1 exon 4 mRNA is expressed in latently infected HPCs.

189 IE1 protein species (IE1x4) is expressed in latently infected HPCs.

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

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

192 attern most closely resembling that found in latently infected human or mouse ganglia in vivo.

193 aboratory mice, infection or immunization of latently infected humans may result in the generation of

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

195 obacterium tuberculosis (M. tuberculosis) in latently infected individuals survives and thwarts the a

196 Moreover, latently infected individuals with DM had diminished lev

197 the increased risk of active tuberculosis in latently infected individuals with DM.

198 potential centers of viral dissemination in latently infected individuals with no evidence of virus

199 ced high levels of proviral transcription in latently infected Jurkat T cells.

200 undantly expressed in IgM(+) WBC from CyHV-3 latently infected koi.

201 EBNA1 depletion from latently infected LCLs results in the loss of cell proli

202 king GAS colonization, elicited lytic EBV in latently infected lymphoblastoid cell lines (LCLs) parti

203 In latently infected marmoset T cells, Herpesvirus saimiri

204 se miRNAs is present at high copy numbers in latently infected memory B cells in vivo, suggesting a r

205 k of fortuitous reactivation of the virus in latently infected memory B cells.

206 ic effector CD4(+) T cells were increased in latently infected mice compared to those in mice infecte

207 When the memory phase was reached, latently infected mice had an LCMV-specific memory T cel

208 The initial replication of LCMV was lower in latently infected mice, and the maturation of dendritic

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

210 as well as in the trigeminal ganglia (TG) of latently infected mice.

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

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

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

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

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

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

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

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

219 (LAT), which plays a key role in maintaining latently infected neurons, but not viral proteins.

220 ajor role may be in silencing viral genes in latently infected neurons, suggests that the virus has e

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

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

223 tone deacetylase inhibitors, as is known for latently infected non-B cell lines, and also selectively

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

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

226 apoptotic protein negatively impacting HHV-8 latently infected primary effusion lymphoma (PEL) cell v

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

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

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

230 ersisted after transfer into immune replete, latently infected recipients and responded if recipient

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

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

233 Currently, one or a few latently infected resting memory CD4 T cells are thought

234 been shown to induce HIV-1 transcription in latently infected resting memory CD4(+) T cells at conce

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

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

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

238 duced the abundance and average life span of latently infected snails.

239 red in its ability to reactivate from either latently infected splenocytes or PECs.

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

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

242 These latently infected T cells represent an extremely small p

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

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

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

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

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

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

249 t epitope exhibit increased functionality in latently infected TG.

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

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

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

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

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

255 cible factor, is frequently elevated in KSHV latently infected tumor cells and contributes to KSHV ly

256 of HIV-1 infection using U1 monocytic cells (latently infected U937 cells with HIV-1).

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

258 In cells latently infected with a herpesvirus, the viral DNA is p

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

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

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

262 asing the cell growth and viability of cells latently infected with EBV.

263 ressed in spleens, livers, or brains of mice latently infected with gammaherpesvirus 68 and found tha

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

265 Lastly, Jurkat T cells latently infected with HIV (JLat cells) were more respon

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

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

268 helial cells, using an endothelial cell line latently infected with KSHV.

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

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

271 majority of asymptomatic individuals who are latently infected with M. tuberculosis (referred to as l

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

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

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

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

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

281 that T(SCM) cells can become productively or latently infected, although the vast majority of T(SCM)

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

283 that recapitulates the in vivo condition of latently infected, resting CD4(+) T lymphocytes.

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 HSV-1 latently infects most humans, causing a variable clinica

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

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

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

292 % difference in capture efficiencies between latently KSHV-infected and uninfected BJAB B lymphoma ce

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

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

295 Treatment of latently KSHV-infected cells with NAM or sirtinol induce

296 lication and maintenance of virus genomes in latently KSHV-infected cells.

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

298 ther individual HSV-infected neurons will be latently or productively infected.

299 e percentage of cells that are productively, latently, or abortively infected.

300 des direct evidence that normal C57BL/6 mice latently possess the capacity to generate humoral respon