ライフサイエンスコーパス: viral latency

1 ect of N-803 by promoting the maintenance of viral latency.

2 ious fate-specification decisions, including viral latency.

3 ms are likely involved in the persistence of viral latency.

4 bitor abolishes the ability of Na to disrupt viral latency.

5 in the case of herpesviruses, by controlling viral latency.

6 ells maintain an activation phenotype during viral latency.

7 s regarding establishment or reactivation of viral latency.

8 -miRNAs expressed from a single locus during viral latency.

9 rvival and KSHV lytic replication to promote viral latency.

10 of the viral life cycle could contribute to viral latency.

11 rus expression and possible establishment of viral latency.

12 uences, may play roles in the maintenance of viral latency.

13 V-specific CD4(+)IFN-gamma(+) T cells during viral latency.

14 vertently wandered into an entirely new area-viral latency.

15 an excellent in vitro model system to study viral latency.

16 terminal repeat (LTR) in the maintenance of viral latency.

17 ANA), a critical factor in the regulation of viral latency.

18 utes to the establishment and maintenance of viral latency.

19 irus-specific CD8+ T cell populations during viral latency.

20 play an important role in the maintenance of viral latency.

21 c immune system components to the control of viral latency.

22 es throughout the body, suggesting sites for viral latency.

23 to be important for R-induced disruption of viral latency.

24 fection in the absence of drug resistance or viral latency.

25 ute HSV-1 infection and the establishment of viral latency.

26 distinct but unknown mechanisms may promote viral latency.

27 anded DNA-reactive antibodies at the peak of viral latency.

28 during lytic infection and reactivation from viral latency.

29 LF1 transcription by YY1 may act to maintain viral latency.

30 ion may therefore modulate the stringency of viral latency.

31 on cellular AKT-mTORC1 signaling to achieve viral latency.

32 type 1 (HSV-1) that can express genes during viral latency.

33 y a key role in regulating the stringency of viral latency.

34 progenitors are an important natural site of viral latency.

35 d plays a critical role in the disruption of viral latency.

36 nscripts in cell lines exhibiting restricted viral latency.

37 cal for correct identification of restricted viral latency.

38 shutoff of transcription that occurs during viral latency.

39 the assay used, or to a particular state of viral latency.

40 nal center response and the establishment of viral latency.

41 ur in some cells, challenging the concept of viral latency.

42 ry CD34(+) HPCs to investigate mechanisms of viral latency.

43 head and neck cancer cells as well as reduce viral latency.

44 imary infection and during reactivation from viral latency.

45 unappreciated aspect of the establishment of viral latency.

46 encoded by the BZLF1 gene, thereby favoring viral latency.

47 fate decision between active replication and viral latency.

48 V68 reactivation during the establishment of viral latency.

49 ticated host immune mechanisms that maintain viral latency.

50 ag without spreading infection in a model of viral latency.

51 ent of lytic infection and reactivation from viral latency.

52 understanding the host biology important to viral latency.

53 iption, which may be important for long-term viral latency.

54 ring primary infection and reactivation from viral latency.

55 viral miRNAs in cellular transformation and viral latency.

56 lays an important role in the maintenance of viral latency.

57 stability of c-Myc to establish and maintain viral latency.

58 ation of HCMV is critical for maintenance of viral latency.

59 ly unspliced viral RNA are a good marker for viral latency.

60 gene expression, promoting host survival and viral latency.

61 ng states in a manner that may be related to viral latency.

62 ation and is required for the maintenance of viral latency.

63 LANA's acidic domain reader is critical for viral latency.

64 der of the animals had persistent tumor-free viral latency.

65 ation and is required for the maintenance of viral latency.

66 roles in gene regulation and maintenance of viral latency.

67 sion to transform human B cells and maintain viral latency.

68 lay an important role in the pathogenesis of viral latency after genital inoculation.

69 arranged WZhet EBV DNA capable of disrupting viral latency, along with the integration of viral DNA i

70 letion of IFN-alpha/beta from wt mice during viral latency also significantly increased viral reactiv

71 r antigen-1 (EBNA1) protein expressed during viral latency, although they have no amino acid similari

72 -1 RNA genome, activating the switch between viral latency and active viral replication.

73 A direct role of viral latency and Ag-specific restimulation in driving t

74 These episomes form the molecular basis for viral latency and are etiologically linked to virus-asso

75 a major locus responsible for maintenance of viral latency and cell transformation.

76 of an antiviral histone chaperone to promote viral latency and cellular immortalization.

77 umor-suppressive TGF-beta pathway to promote viral latency and contribute to malignant cellular trans

78 ene expression may be coordinated to promote viral latency and control lytic-cycle entry.

79 LMP2A) of EBV plays a key role in regulating viral latency and EBV pathogenesis by functionally mimic

80 T cells may contribute to the maintenance of viral latency and identified a novel SMAC mimetic/IAP in

81 ctor CD4 T cells are critical for control of viral latency and in immune therapies for virus-associat

82 emonstrate that disease enhancement requires viral latency and is not due to active virus stimulation

83 entral role in regulating the switch between viral latency and lytic replication.

84 tal for understanding the transition between viral latency and lytic replication.

85 ng latency by controlling the switch between viral latency and lytic replication.

86 an understanding of the molecular basis for viral latency and persistence is paramount to controllin

87 cancer depend on understanding what controls viral latency and persistence.

88 lished, the molecular mechanisms that govern viral latency and prevent oncogenic progression remain p

89 Developing therapies to reverse viral latency and prevent spread is paramount for the HI

90 L-6 is produced in functional amounts during viral latency and promotes the growth of these cells, me

91 e model may provide a valuable tool to study viral latency and reactivation as well as evaluate HCMV

92 17RA signaling supports the establishment of viral latency and reactivation in the spleen and periton

93 been useful in elucidating the mechanisms of viral latency and reactivation, omics approaches have pr

94 a microfluidic-based human neuronal model of viral latency and reactivation, we found that inhibition

95 ences various cellular processes crucial for viral latency and reactivation, yet the precise mechanis

96 ected HPCs from TGF-beta-mediated effects on viral latency and reactivation.

97 ssion of HSV-1 IE genes that in turn control viral latency and reactivation.

98 ration, differentiation, transformation, and viral latency and reactivation.

99 nipulates host signaling networks to mediate viral latency and reactivation.

100 e virus-host interactions that contribute to viral latency and reactivation.

101 der ages supports a natural history model of viral latency and reactivation.

102 test impact on regulating the switch between viral latency and replication.

103 RTA plays a critical role in the control of viral latency and suggests that latency is a determinant

104 ed to suppress viral replication and promote viral latency and that MCPyV ALTO must be silenced for M

105 nt to proviral HIV-1, for the maintenance of viral latency and the control of viral reactivation.

106 owledge of the HDAC isoforms contributing to viral latency and the development of inhibitors specific

107 V-1) and herpesviruses, in large part due to viral latency and the evolution of resistance to existin

108 l herpesviruses is their biphasic life cycle-viral latency and the productive lytic cycle-and it is w

109 tors, is necessary and sufficient to disrupt viral latency and to initiate the viral lytic cycle.

110 wherein IRF-7 restricts the establishment of viral latency and viral reactivation.

111 ly limited to chronic infection dominated by viral latency and was less relevant for lytic replicatio

112 of virus-encoded miRNA in the regulation of viral latency and will help guide the development of nov

113 fic for herpesviruses may vary with sites of viral latency and with host age.

114 t play important roles in viral replication, viral latency, and immune escape.

115 t play important roles in viral replication, viral latency, and immune escape.

116 B cells serve as the major reservoir for viral latency, and it is hypothesized that periodic reac

117 t on viral gene expression, establishment of viral latency, and other aspects of the replication cycl

118 t that the sumoylation of Z helps to promote viral latency, and that EBV-PK inhibits Z sumoylation du

119 vities of other EBNA1 promoters, the type of viral latency, and the cell type.

120 virus, the rapid establishment of persistent viral latency, and the challenges associated with induct

121 inked to transcriptional activation, cancer, viral latency, and viral integration.

122 -lived cellular subsets and establishment of viral latency, and viral rebound with return to pretreat

123 ansion of high affinity T cells specific for viral latency antigens involved in cell transformation.

124 nally silent, but mechanisms responsible for viral latency are insufficiently clear.

125 of MHV68-infected splenocytes at the peak of viral latency are plasma cells (ca. 15% at day 14 and ca

126 hase-variation (RPV) of pathogenic bacteria, viral latency as observed in some bacteriophage and HIV,

127 ed cells in vivo led to a severe ablation of viral latency, as assessed on both days 16 and 42 postin

128 es in the UL144 promoter, in contrast to the viral latency-associated gene LUNA, which we also show i

129 rs, invariably expressing high levels of the viral latency-associated nuclear antigen (LANA) protein.

130 As in human KS, all tumor cells express the viral latency-associated nuclear antigen (LANA).

131 herpesvirus (KSHV) episomes are coated with viral latency-associated nuclear antigen (LANA).

132 LANA binds both the viral latency-associated origin of replication and the h

133 host transcriptional repressor KAP1 and the viral latency-associated protein LANA-1 to mediate globa

134 For HSV, we have shown previously that the viral latency-associated transcript (LAT) promotes lytic

135 e found to support latency and expression of viral latency-associated transcripts and to undergo reac

136 ralin (dithranol) as novel LRAs that reverse viral latency at low micromolar concentrations in multip

137 and off rates we observe may be relevant to viral latency because viral activation requires sustaine

138 promoter for PrV LAT gene expression during viral latency but is not required for such activity duri

139 + T cells play a crucial role in controlling viral latency by generating diverse memory responses in

140 how that the KSHV latent gene vFLIP promotes viral latency by inhibiting viral lytic replication.

141 The viral LMP2A protein mediates viral latency by mimicking a constitutively activated B-

142 ilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral

143 ng the lytic cycle and also help to maintain viral latency by preventing viral reactivation.

144 vator expression and promotes maintenance of viral latency by targeting the viral polycistronic trans

145 The EBNA2-responsive enhancer in the viral latency C promoter (Cp) binds two cellular factors

146 Viral latency can be considered a metastable, nonproduct

147 herpesvirus latency in vivo and suggest that viral latency can be disseminated by cellular proliferat

148 cation, the establishment and maintenance of viral latency, cell survival, and innate and adaptive im

149 nt for EBNA2-mediated transactivation of the viral latency Cp.

150 Beyond viral latency, CXA has the potential to advance many stu

151 stochastic fluctuations in Tat influence the viral latency decision.

152 CTL depletion reversed the viral latency deficit.

153 M deficiency attenuated the establishment of viral latency due to compromised differentiation of ATM-

154 of intact proviruses with features of deeper viral latency during prolonged antiretroviral therapy, a

155 of the molecular and cellular mechanisms of viral latency, efforts to accurately assess the size and

156 ction of K3 appears to be CTL evasion during viral latency expansion.

157 n requires transition from a program of full viral latency gene expression (latency III) to one that

158 Our study reveals that a viral latency gene functions within a distinct subset of

159 nes are transcriptionally upregulated, while viral latency genes are downregulated ahead of expressio

160 , including those for all the other type III viral latency genes as well as cellular genes responsibl

161 BV transforms RBLs through the expression of viral latency genes, and these genes alter host transcri

162 ell immortalization depends on expression of viral latency genes, as well as the regulation of host g

163 -Barr virus (EBV) requires the expression of viral latency genes, latency can be maintained with a ne

164 ylation patterns that restrict expression of viral latency genes.

165 n of Cp activity during the establishment of viral latency has previously been proposed.

166 knowledge of the viral processes that govern viral latency has shed light upon the potential mechanis

167 expression in EBV-positive tumors, caused by viral latency, however, makes antiviral therapy alone in

168 ort a highly transforming form (type III) of viral latency; however, long-term EBV infection in immun

169 EBV cancers typically exhibit viral latency; however, the production and release of EB

170 promoter switching governs reactivation from viral latency in a context-specific manner.

171 ntrol and Z-KO viruses established long-term viral latency in all infected animals.

172 immediate-early protein, BRLF1, can disrupt viral latency in an epithelial cell-specific fashion.

173 c transcription factor Pax5 helps to promote viral latency in B cells by blocking Z function.

174 nib or idelalisib.IMPORTANCE EBV establishes viral latency in B cells.

175 E EBV establishes several different types of viral latency in B cells.

176 dundant mechanisms to establish and maintain viral latency in B cells.

177 c switch protein, thereby ensuring continued viral latency in B lymphocytes.

178 required for the successful establishment of viral latency in CD34(+) cells, as pharmacological inhib

179 both pUL133 and pUL138 function in promoting viral latency in CD34(+) hematopoietic progenitor cells

180 own about the SEC subtypes that help reverse viral latency in CD4(+) T cells.

181 ed this hypothesis by kinetically monitoring viral latency in CD40(+) and CD40(-) B cells from CD40(+

182 gamma-herpesvirus-68 (gammaHV68) establishes viral latency in dendritic cells (DCs).

183 ions as a major factor in the maintenance of viral latency in Epstein-Barr virus (EBV)-positive Burki

184 As monocytes are believed to be a site of viral latency in HCMV carriers and reactivated virus is

185 stand EBV-induced B-cell immortalization and viral latency in humans.

186 role in the establishment and maintenance of viral latency in infected animals.

187 uctively infected cells but does not disrupt viral latency in latently infected cells.

188 bute to the establishment and maintenance of viral latency in lymphocytes.

189 viral ICP0 messenger RNA, thereby promoting viral latency in mice.

190 ssociation between the B cell life cycle and viral latency in that the virus preferentially establish

191 4(+) cell population is an important site of viral latency in the naturally infected human host.

192 increases dramatically following the peak of viral latency in the spleen.

193 enuation of the germinal center response and viral latency in the spleen.

194 this mechanism is unlikely to be a driver of viral latency in this cell type.

195 neurons, and thus favor the establishment of viral latency in those cells, may be found in the cell-s

196 However, ApoE expression did not affect viral latency in vivo, implying a novel viral life cycle

197 vity of vIL-6 involving VKORC1v2 may promote viral latency (in PEL cells) and productive replication

198 otein that is expressed predominantly during viral latency, in most KS spindle cells and in cell line

199 is critical for establishing and maintaining viral latency, in part, through regulating host cell sig

200 Viral latency, in which a virus genome does not replicat

201 transcript, FoxP3, continued to decrease as viral latency increased and as the leukocytosis phase of

202 nt samples presenting with restricted type I viral latency, indicating that EBV latency proteins are

203 th HTLV-1 Tax-LTR-mediated transcription and viral latency, indicating that they may act as general t

204 t EBNA1 gene transcription during restricted viral latency initiates at multiple sites downstream of

205 Viral latency is a central strategy by which herpesvirus

206 Although viral latency is a critical factor in this persistence,

207 Viral latency is a long-term pathogenic condition in pat

208 Understanding how viral latency is disrupted is a central issue in herpesv

209 Viral latency is established when the expression of the

210 the uncontrolled expansion of leukocytes as viral latency is established.

211 +) T cell effector mechanisms in maintaining viral latency is explained as follows: (1) a subset of n

212 m kinases in control of virus expression and viral latency is important for Kaposi sarcoma-associated

213 How viral latency is maintained in tumors or in memory B cel

214 Viral latency is maintained, in part, by virus-specific

215 cleus, suggesting that their contribution to viral latency is purely nuclear.

216 Understanding the molecular basis for viral latency is the key first step.

217 tic (productive) replication, in addition to viral latency, is believed to play a critical role.

218 The existence of viral latency limits the success of highly active antire

219 vector flanked by boundary elements from the viral latency locus showed high, persistent reporter gen

220 in the face of therapy has been explained by viral latency, lowered effectiveness of drugs in some an

221 rther evaluate the role of CD8(+) T cells in viral latency maintenance.

222 Some viral latency may be related to DNA methylation.

223 Pharmacological disruption of viral latency may expose HIV-1-infected cells to host im

224 During the early phase of viral latency, MHV68-YFP efficiently marked latently inf

225 sed by a combination of spillover events and viral latency or persistence in survivors.

226 s to augment ART with therapies that reverse viral latency, paired with immunotherapies to clear infe

227 e ability of Z expression vectors to disrupt viral latency, presumably because expression of Z under

228 We propose that viral latency products may repress via stalling key medi

229 The viral latency program of KSHV is central to persistent i

230 life-long infection in humans, with distinct viral latency programs predominating during acute and ch

231 fragments BamHI W and BamHI Z that disrupts viral latency, prompted us to determine at the nucleotid

232 omponent of licorice, reduces synthesis of a viral latency protein and induces apoptosis of infected

233 The first viral latency protein expressed, EBNA-LP, is essential f

234 iscernible evolution, providing evidence for viral latency rather than drug failure.

235 h complex patterns of gene expression during viral latency, reactivation, and de novo infection.

236 Studies of viral latency, reactivation, and the cellular effects of

237 that HCF-1 is an important component of the viral latency-reactivation cycle and that it is regulate

238 ls to immune-mediated clearance by reversing viral latency, recent work shows that these cells also r

239 The viral latency related gene, which is abundantly expresse

240 states are virtually indistinguishable, and viral latency remains a topic of ongoing research and de

241 While viral latency remains one of the biggest challenges for

242 Viral latency remains the most significant obstacle to H

243 Disruption of viral latency requires transcriptional activation of the

244 ection interfering with the establishment of viral latency.SignificanceThe expression of epigenetic f

245 role in the bacterium-mediated disruption of viral latency similar to that of previously reported res

246 ked to the virus and are associated with the viral latency status.

247 >90% expressed gene products associated with viral latency (T0.7 transcript).

248 in immune deficient mice (huNSG) results in viral latency that can be reactivated following G-CSF tr

249 During viral latency, the latency-associated nuclear antigen (L

250 y shielded from host immune responses due to viral latency, these cells do, on closer examination wit

251 Protein-mediated viral latency through cellular SCF E3 ligase targeting o

252 ng, participates in the process of switching viral latency to lytic replication.

253 necessary and sufficient for the switch from viral latency to lytic replication.

254 ALT is expressed antisense to the major viral latency transcripts encoding LANA as well as the v

255 In both cases, forms of viral latency (type I and type IIB) were observed that a

256 o study the establishment and maintenance of viral latency, viral reactivation, and changes in the fu

257 After viral latency was established, transcorneal epinephrine

258 In contrast, no defect in viral latency was observed in TLR3(-/-) mice.

259 r active in the type I program of restricted viral latency was recently identified and shown to resid

260 EBER1 mRNA, a consistent marker of viral latency, was positive in all PEL cases, although a

261 f lymphocyte subsets in the establishment of viral latency, we analyzed the latent SVV transcriptome

262 he maintenance and possibly establishment of viral latency, which may contribute to pathogenesis of P

263 uppressing HIV-1 transcription and promoting viral latency, which may serve as promising gene targets

264 biological screening in a cellular model of viral latency with virtual screening is useful for the i

265 ifferent CD8 effector mechanisms to maintain viral latency, with some requiring IFN-gamma and others

266 Varicella severity and viral latency within sensory ganglia were comparable in

267 Because JQ1 activates viral latency without inducing global T cell activation,

268 open reading frame deletion mutant maintain viral latency yet fail to efficiently reactivate.