ライフサイエンスコーパス: viral latency

1 fate decision between active replication and viral latency.

2 rvival and KSHV lytic replication to promote viral latency.

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

4 rus expression and possible establishment of viral latency.

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

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

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

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

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

10 V68 reactivation during the establishment of viral latency.

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

12 utes to the establishment and maintenance of viral latency.

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

14 ticated host immune mechanisms that maintain viral latency.

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

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

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

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

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

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

21 during lytic infection and reactivation from viral latency.

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

23 ion may therefore modulate the stringency of viral latency.

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

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

26 progenitors are an important natural site of viral latency.

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

28 nscripts in cell lines exhibiting restricted viral latency.

29 cal for correct identification of restricted viral latency.

30 shutoff of transcription that occurs during viral latency.

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

32 ent of lytic infection and reactivation from viral latency.

33 understanding the host biology important to viral latency.

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

35 ring primary infection and reactivation from viral latency.

36 viral miRNAs in cellular transformation and viral latency.

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

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

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

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

41 gene expression, promoting host survival and viral latency.

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

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

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

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

46 roles in gene regulation and maintenance of viral latency.

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

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

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

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

51 ells maintain an activation phenotype during viral latency.

52 s regarding establishment or reactivation of viral latency.

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

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

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

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

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

58 -1 RNA genome, activating the switch between viral latency and active viral replication.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Viral latency can be considered a metastable, nonproduct

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

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

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

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

112 stochastic fluctuations in Tat influence the viral latency decision.

113 CTL depletion reversed the viral latency deficit.

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

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

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

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

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

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

120 ylation patterns that restrict expression of viral latency genes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 4(+) cell population is an important site of viral latency in the naturally infected human host.

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

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

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

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

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

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

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

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

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

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

154 Viral latency is a central strategy by which herpesvirus

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

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

157 Viral latency is established when the expression of the

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

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

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

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

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

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

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

165 Some viral latency may be related to DNA methylation.

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

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

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

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

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

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

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

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

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

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

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

177 While viral latency remains one of the biggest challenges for

178 Viral latency remains the most significant obstacle to H

179 Disruption of viral latency requires transcriptional activation of the

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

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

182 >90% expressed gene products associated with viral latency (T0.7 transcript).

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

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

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

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

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

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

189 After viral latency was established, transcorneal epinephrine

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

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

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

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

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

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

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

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

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

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