ライフサイエンスコーパス: HVS

1 HVS encodes seven small RNAs (HSURs) of unknown function

2 HVS is an oncogenic gammaherpesvirus that causes acute T

3 HVS triggers a distinctive retinopathy with a central re

4 HVS-related retinopathy improved in all patients after p

5 hondrial DNA results of 213 individuals (151 HVS-I sequences) from the northeast, central, southeast

6 Only one HVS (US 708, HVS 2) is a compact helium star.

7 s likely to receive surgery at a HVH or by a HVS compared to urban patients.

8 with lower odds of surgery at a HVH or by a HVS.

9 In addition, HVS Deltaorf14 was nononcogenic in common marmosets.

10 In addition, HVS deltaSTP/v-ras-immortalized T cells showed a high le

11 r each of Ext-3, Ext-5, F-6, and F-7 against HVS-2 with IC(50) of 101.23, 68.83, 4.88, 3.24 mug/mL an

12 (50) value of the standard acyclovir against HVS-2 was 83.19 mug/mL and IC(50) value of the standard

13 This allows HVS-based vectors to stably transduce a dividing cell po

14 iscuss and contrast the AUC with alternative HVS, including the time-averaged AUC, duration of viremi

15 ommon marmosets, while HVS deltaSTP-C488 and HVS deltaTip were nononcogenic.

16 to interact with cellular type D cyclins and HVS v-cyclin.

17 e factors associated with surgery by HVH and HVS.

18 lead to a hyperviscosity syndrome (HVS) and HVS-related retinopathy.

19 Interaction between Integrator and HVS primary miRNA (pri-miRNA) substrates that contain on

20 Although KSHV and HVS are related members of the rhadinovirus subgroup of

21 The KSHV and HVS LANAs have also been shown to be required for mainte

22 Epstein-Barr virus membrane antigen p140 and HVS p160, (ii) HVS and cellular type D cyclins, (iii) HV

23 Finally, HVS deltaSTP/v-ras and HVS deltaSTP/c-ras each induced lymphoma in one of two c

24 itive T lymphocytes, HVS deltaSTP/c-ras- and HVS deltaSTP/v-ras-immortalized cells were principally C

25 these two functional domains of the TEAS and HVS genes resulted in a novel enzyme capable of synthesi

26 The relative ratio of the TEAS and HVS reaction products was also influenced by the source

27 he vitreous of the eye and is induced before HVS regression in the first postnatal week.

28 ons confirmed the close relationship between HVS physiology and retinal neurovascular development.

29 his cis-acting element is sufficient to bind HVS ORF73 from strains C488 and A11, and plasmids contai

30 ets resulted in fulminant lymphoma with both HVS/Tip mSH3B and wild-type HVS.

31 for TS and DHFR enzymes are also encoded by HVS (ORF70 and ORF2), both occur at different genomic lo

32 A protein encoded by HVS known as Tip-484 (for tyrosine kinase interacting pr

33 ate that, due to the sequestration of Lck by HVS Tip, T cell receptor (TCR) stimulation fails to acti

34 iri-immortalized primary CD4(+) T cells (CD4/HVS), which resemble activated primary T cells.

35 However, a TR-deleted HVS bacterial artificial chromosome can form replication

36 on the functions of the recently discovered HVS miRNAs, called miR-HSURs.

37 The distorted HVS regression might result from retinal hyperoxia or do

38 In the absence of Arf, failed HVS regression causes a pathological process that resemb

39 Finally, HVS deltaSTP/v-ras and HVS deltaSTP/c-ras each induced l

40 city experiments, the Michaelis constant for HVS was 3.5 microM, while CH3 and CH4 exhibited smaller

41 The patients were evaluated for HVS-related retinopathy, and hemodynamic changes in a ma

42 like sequence (miRNA 3' box) downstream from HVS pre-miRNAs that is essential for miRNA biogenesis.

43 for tyrosine kinase interacting protein from HVS strain 484) is required for this transformation.

44 ull-length form (residues 1-187) of Tip from HVS strain C484.

45 Furthermore, HVS terminal repeats (TRs) contain a cis-acting sequence

46 Analysis of the gammaHV68, HVS, EBV, and KSHV genomes demonstrated that each of the

47 However, HVS/Tip mSH3B produced greater infiltration of affected

48 We examined embryonic and fetal human HVS using a variety of techniques to gain new insights i

49 Our results support the view that the human HVS, like the choriocapillaris, develops by hemo-vasculo

50 re less likely to receive surgery from a HVH/HVS.

51 f14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in the o

52 rus membrane antigen p140 and HVS p160, (ii) HVS and cellular type D cyclins, (iii) HVS and cellular

53 (ii) HVS and cellular type D cyclins, (iii) HVS and cellular G protein-coupled receptors, and (iv) H

54 Consistently, inhibition of miR-HSUR5-3p in HVS-infected cells decreases their proliferation.

55 Furthermore, the p56lck kinase activity in HVS-infected human peripheral blood T lymphocytes was at

56 ri U RNAs), that are abundantly expressed in HVS-transformed, latently infected marmoset T cells but

57 pesvirus type 4 and a similar motif found in HVS ORF12.

58 the ARE-binding proteins hnRNP D and HuR in HVS-transformed T cells using a new cross-linking assay.

59 ential for transformation and oncogenesis in HVS-infected cells.

60 f is degraded by an ARE-dependent pathway in HVS-transformed T cells, suggesting that HVS may take ad

61 viously known to bind a homologous region in HVS ORF57.

62 8 TR element are maintained and replicate in HVS C488 ORF73-expressing cells.

63 ) are the most abundant viral transcripts in HVS-transformed, latently infected T cells but are not r

64 llular G protein-coupled receptors, and (iv) HVS.

65 pression from a range of both early and late HVS promoters, depending on the target gene.

66 zed CD4- CD8+ single-positive T lymphocytes, HVS deltaSTP/c-ras- and HVS deltaSTP/v-ras-immortalized

67 3.28 vs 2.30, P < .001), as well as the mean HVS score (4.12 vs 3.19, P < .001).

68 f infected marmosets for more than 5 months, HVS Deltaorf14 did not persist at a high level in vivo.

69 cells transformed with wild-type or a mutant HVS lacking the most highly conserved HSURs, HSURs 1 and

70 bits inoculated with Tip-484 deletion mutant HVS.

71 escued after transduction of deletion-mutant-HVS-transformed cells with a lentiviral vector carrying

72 In contrast to other nononcogenic HVS mutant viruses which were repeatedly isolated from p

73 The LYVE-1 expression was detected on normal HVS between E12.5 and P14.

74 oded by other gammaherpesviruses (gene 16 of HVS and KSHV and the BHRF1 gene of EBV).

75 stetraprolin induced following activation of HVS-transformed T cells, but even in such stimulated cel

76 at the signaling and targeting activities of HVS Tip rely on functionally and genetically separable m

77 stent with the lack of oncogenic activity of HVS subgroup B viruses, STP-B was deficient for transfor

78 Orf73, encoding the nuclear antigen of HVS, is the positional homolog of the LANA gene, and the

79 t sequence is a determinant of the degree of HVS STP transforming activity.

80 Despite the pronounced effects of HVS Tip on T cell signal transduction, the details of it

81 ng signal (3' box), generates the 5' ends of HVS pre-miRNA hairpins.

82 of orf14 in transformation, a mutant form of HVS (HVS Deltaorf14) was constructed with a deletion in

83 We constructed a mutant form of HVS in which prolines in the SH3B motif of Tip were alte

84 us, the signaling and targeting functions of HVS Tip rely on two functionally and genetically separab

85 hat may contribute to the immunopathology of HVS infection.

86 However, physiological mechanisms of HVS regression and their correlation with developmental

87 rstanding of the physiological mechanisms of HVS regression in normal and diseased eyes, which is not

88 CT) and OCT angiography (OCTA) monitoring of HVS regression in wild-type and retinal degeneration 10

89 ging platform for longitudinal monitoring of HVS regression, further OCT/OCTA study may lead to in-de

90 t ras can substitute for the STP oncogene of HVS C488 to allow immortalized growth of primary lymphoi

91 ant herpesvirus in which the STP oncogene of HVS was replaced by R1 immortalized T lymphocytes to int

92 ant herpesvirus in which the STP oncogene of HVS was replaced with K1, immortalized primary T lymphoc

93 These results demonstrate that orf14 of HVS is not required for replication but is required for

94 However, the function of ORF73 of HVS has not been thoroughly investigated.

95 e below the level of detection in a panel of HVS-transformed CD8(+) cells with potent HIV-1 inhibitor

96 The transforming potential of HVS Deltaorf14 was tested in cell culture and in common

97 P is required for the oncogenic potential of HVS, we investigated the functional consequence of K1 ex

98 Here we assess the potential of HVS-based vectors for the generation of induced pluripot

99 ents confirmed that the 3' end processing of HVS pre-miRNAs also depends on Integrator activity.

100 ation, we constructed recombinant strains of HVS C488 in which the STP-C488 oncogene was replaced wit

101 A better understanding of HVS biology will help advance our knowledge of virus-ind

102 The spike component of HVSs was associated with fast field oscillations (400-60

103 rces determined the amplitude variability of HVSs and sleep spindles.

104 investigate the effects of plasmapheresis on HVS-related retinopathy and retinal hemodynamic paramete

105 ncer, viral miRNAs from the highly oncogenic HVS might also be important for transformation.

106 Only one HVS (US 708, HVS 2) is a compact helium star.

107 ion of p53 tetramerization by either LANA or HVS-encoded ORF73, suggesting that p53 inactivation may

108 ntrasts with the recent description of other HVS-transformed CD4+ T cells that provide B cell help pr

109 ost favored ejection mechanism for the other HVSs.

110 Through the interactions with Lck and p80, HVS Tip modulates diverse T-cell functions, which leads

111 Parental HVS subgroup C strain 488 immortalized common marmoset T

112 Parental HVS subgroup C strain 488 immortalized common marmoset T

113 es and high voltage spike-and-wave patterns (HVSs).

114 -2) knockout mice with abnormally persistent HVS were examined.

115 gly, in contrast to snRNA 3' end processing, HVS pre-miRNA 3' end processing by Integrator can be unc

116 lation or repress Vegf expression to promote HVS involution and prevent PHPV.

117 Recombinant HVS deltaSTP/v-ras immortalized primary common marmoset

118 ld-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras did so with low efficiency.

119 hat the RRV26-95 DHFR more closely resembles HVS DHFR (74% similarity) than KSHV DHFR (55% similarity

120 Plasmapheresis is effective in reversing HVS-related retinopathy and in reducing abnormal venous

121 acting protein (Tip) of Herpesvirus saimiri (HVS) activates the lymphoid-specific member of the Src f

122 ed cyclin (v-cyclin) of herpesvirus saimiri (HVS) and 31% identity and 53% similarity to human cellul

123 by the DNA tumor virus herpesvirus saimiri (HVS) and designated tyrosine kinase interacting protein

124 orming protein (STP) of herpesvirus saimiri (HVS) and of K1 of KSHV, other members of the gamma-2 or

125 The lymphotropic Herpesvirus saimiri (HVS) causes acute leukemia, T-cell lymphoma, and death i

126 Herpesvirus saimiri (HVS) encodes seven Sm-class small nuclear RNAs, called H

127 ing frame 14 (orf14) of herpesvirus saimiri (HVS) exhibits significant homology with mouse mammary tu

128 ected marmoset T cells, Herpesvirus saimiri (HVS) expresses six microRNAs (known as miR-HSURs [H. sai

129 th the right end of the herpesvirus saimiri (HVS) genome and more limited homology to the left end of

130 The herpesvirus saimiri (HVS) immediate-early gene product encoded by open readin

131 Herpesvirus saimiri (HVS) infects a range of human cell types with high effic

132 Herpesvirus saimiri (HVS) is a gamma-herpesvirus that expresses Sm class U RN

133 Herpesvirus saimiri (HVS) is a T-cell-specific transforming and oncogenic vir

134 Herpesvirus saimiri (HVS) is an oncogenic gamma-herpesvirus that produces mic

135 Herpesvirus saimiri (HVS) is an oncogenic, lymphotropic, gamma-herpesvirus th

136 ) of the T lymphotropic Herpesvirus saimiri (HVS) is constitutively present in lipid rafts and intera

137 Herpesvirus saimiri (HVS) is divided into three subgroups, A, B, and C, based

138 acting protein (Tip) of herpesvirus saimiri (HVS) is required for binding to the cellular Src family

139 , including the gamma-2 herpesvirus saimiri (HVS) of New World squirrel monkeys.

140 minal repeats (TR) from herpesvirus saimiri (HVS) renders it unable to produce infectious virus or ge

141 by the DNA tumor virus herpesvirus saimiri (HVS) strain 484, designated tyrosine kinase-interacting

142 ogene, called STP-A, of herpesvirus saimiri (HVS) subgroup A is not required for viral replication bu

143 STP oncoproteins of the herpesvirus saimiri (HVS) subgroup A strain 11 and subgroup C strain 488 are

144 Mutant forms of herpesvirus saimiri (HVS) subgroup C strain 488 with deletions in either STP-

145 The herpesvirus saimiri (HVS) tyrosine kinase-interacting protein (Tip), required

146 d by two herpesviruses, herpesvirus saimiri (HVS) which can transform blood lymphocytes and induce ma

147 Sm class are encoded by Herpesvirus saimiri (HVS), a gamma Herpesvirus that causes aggressive T cell

148 T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding (nc) RNA, HSUR 1, specifi

149 s human herpesvirus 8), herpesvirus saimiri (HVS), and Epstein-Barr virus (EBV).

150 Herpesvirus saimiri (HVS), another gamma-2-herpesvirus, primarily infects New

151 genome in RRV26-95 and herpesvirus saimiri (HVS), but in KSHV the DHFR gene is displaced 16,069 nucl

152 herpesvirus (KSHV) and herpesvirus saimiri (HVS), has been shown to encode a latency-associated nucl

153 orming protein (STP) of herpesvirus saimiri (HVS), Kaposi's sarcoma-associated herpesvirus (KSHV) con

154 onors by infection with Herpesvirus saimiri (HVS), to evaluate functional properties of these immorta

155 olog of KSHV ORF57 from herpesvirus saimiri (HVS), we determined the crystal structure of the globula

156 ded by the lymphotropic Herpesvirus saimiri (HVS), we determined the specific sequence and structural

157 The Tip protein of herpesvirus saimiri (HVS), which is a T-lymphotropic tumor virus, interacts w

158 emonstrated that Tip of herpesvirus saimiri (HVS), which is a T-lymphotropic tumor virus, is constitu

159 -1 and CAF derived from herpesvirus saimiri (HVS)-transformed CD8(+) cells inhibited HIV-1 infection

160 e 6 (ORF6) and ORF31 of herpesvirus saimiri (HVS).

161 eading frame (ORF) from herpesvirus saimiri (HVS).

162 elated gammaherpesvirus herpesvirus saimiri (HVS).

163 ymphotropic tumor virus herpesvirus saimiri (HVS).

164 STP-C488 (STP of herpesvirus saimiri [HVS] group C strain 488 [C488]) is the only virus-encode

165 n Scale (EDS) or Heightened Vigilance Scale (HVS), adjusting for age, sex, race/ethnicity, household

166 tochondrial SNPs and hypervariable sequence (HVS) 1, Tamil castes have higher affinity to eastern Asi

167 By deep sequencing, we identified six HVS microRNAs (miRNAs) that are derived from three hairp

168 cellular currents underlying sleep spindles, HVSs, and evoked responses result from activation of int

169 sources were similar during sleep spindles, HVSs, and thalamic-evoked responses, although their rela

170 Hypervelocity stars (HVSs) travel with velocities so high that they exceed th

171 owever, alternative historical VL summaries (HVS) may better answer the research question of interest

172 which can lead to a hyperviscosity syndrome (HVS) and HVS-related retinopathy.

173 Hyoscyamus muticus vetispiradiene synthase (HVS) gene and by characterization of the resulting chime

174 Hyoscyamus muticus vetispiradiene synthase (HVS), a chimeric 5-epi-aristolochene synthase (CH3), and

175 l regression of the hyaloid vascular system (HVS) in the mouse eye.

176 The hyaloid vascular system (HVS) is a transient network nourishing developing eyes a

177 The hyaloid vascular system (HVS) is known to have an important role in eye developme

178 cell biology in the hyaloid vascular system (HVS) of the developing eye.

179 opment of the human hyaloid vascular system (HVS) remains unclear.

180 These results demonstrate that HVS utilizes a novel signaling protein, ORF5, to activat

181 We demonstrate that HVS-based exogenous delivery of Oct4, Nanog, and Lin28 c

182 processing assays in vitro demonstrated that HVS does not utilize the Microprocessor complex that gen

183 These results indicate that HVS-immortalization of CD4+ lymphocytes may produce T ce

184 udy Adolescent Master Protocol, we show that HVS and their associations with full-scale intelligence

185 We show that HVS miRNA biogenesis relies on cis-acting elements speci

186 In this report, we show that HVS ORF73 may be important for episome persistence and c

187 in HVS-transformed T cells, suggesting that HVS may take advantage of the host ARE-mediated mRNA dec

188 The HVS STP-C488 P10-->R mutant was deficient in human T-lym

189 erentiation trials suggest that although the HVS-derived putative iPCs are capable of differentiation

190 g the frequency of unfair treatment, and the HVS, measuring how often individuals anticipate or prepa

191 mon marmoset lymphocytes immortalized by the HVS/Tip mSH3B mutant displayed increased expression of H

192 ns C488 and A11, and plasmids containing the HVS C488 TR element are maintained and replicate in HVS

193 vestigate whether LYVE-1 is expressed in the HVS and how it is associated with the vascular structure

194 s that map to the host genome but few in the HVS genome.

195 In the HVS, Arf expression in perivascular cells may block thei

196 there is no report on its expression in the HVS.

197 farther diverged from human DHFR than is the HVS version, implying that they were probably acquired a

198 Moreover, the HVS episome is able to persist and provide prolonged tra

199 roducts of the tobacco enzyme, exon 6 of the HVS gene conferred specificity for the predominant react

200 Nucleotide sequence analysis of the HVS genome revealed an open reading frame with 22% amino

201 The transforming potentials of the HVS mutants were tested in cell culture and in common ma

202 ng the embryogenesis and pathogenesis of the HVS, it also leads to a completely natural model in whic

203 Further analysis of the HVS-derived putative iPCs showed some degree of reprogra

204 95% CI: 1.62-1.87) and higher scores on the HVS (adjusted OR: 1.61, 95% CI: 1.51-1.72).

205 ORF73, the HVS homologue of LANA, is shown to bind both p53 and pRb

206 s study provides the first evidence that the HVS contains a LYVE-1(+) cellular component in both phys

207 homologous to HVS and KSHV ORFs and used the HVS/KSHV numbering system to designate these ORFs.

208 interleukin-2-independent growth, while the HVS Deltaorf14 mutant did not produce such a growth tran

209 episome persistence and colocalizes with the HVS genomic DNA on metaphase chromosomes.

210 rf, perivascular cells accumulate within the HVS and prevent its involution.

211 Therefore, HVS Tip uniquely targets the retromer complex to impair

212 d that these activities likely contribute to HVS-mediated lymphoid cell immortalization in culture an

213 63 open reading frames (ORFs) homologous to HVS and KSHV ORFs and used the HVS/KSHV numbering system

214 he v-cyclin of the T-lymphocyte-transforming HVS in its specificity for association with cdk6 and in

215 dependent growth as efficiently as wild-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras

216 Wild-type HVS produced fatal lymphoma within 19 to 20 days of expe

217 mphoma with both HVS/Tip mSH3B and wild-type HVS.

218 erating lymphoid cells compared to wild-type HVS.

219 compared to cells immortalized by wild-type HVS.

220 The mutant virus, HVS/Tip mSH3B, retained its ability to immortalize commo

221 imental infection of common marmosets, while HVS deltaSTP-C488 and HVS deltaTip were nononcogenic.

222 Infection of T cells with HVS or expression of recombinant Tip-484 significantly i

223 ot altered in T cells latently infected with HVS mutants lacking HSURs 1 and 2.

224 lize with p53 in human T cells infected with HVS, and in cells overexpressing both ORF73 and p53, as

225 Nine patients with HVS due to WM were studied.

226 gammaHV68 shares with HVS and KSHV ORFs homologous to a complement regulatory

227 wth as efficiently as wild-type HVS C488 (wt HVS), while recombinant HVS deltaSTP/c-ras did so with l

228 Whereas wt HVS immortalized CD4- CD8+ single-positive T lymphocytes