ライフサイエンスコーパス: JC virus

1 ticles (VLPs) derived from the human polyoma JC virus.

2 ntact cells, and cannot distinguish BKV from JC virus.

3 ic recognition of a human neurotropic virus, JC virus.

4 from an oligodendrocyte infection caused by JC virus.

5 sus macaque simian virus 40 (SV40) and human JC virus.

6 brain cells, termed oligodendrocytes, by the JC virus.

7 urine was 400 times higher for BK virus than JC virus.

8 der caused by oligodendrocyte destruction by JC virus.

9 activation and neurotropic transformation of JC virus.

10 Less than 5% of cases are attributed to the JC virus.

11 brain disease caused by reactivation of the JC virus.

12 cal leukoencephalopathy, associated with the JC virus, a human polyomavirus.

13 The virus was named JC virus after the initials of the patient.

14 us disease in immunocompromised individuals, JC virus and BK virus, encode miRNAs with the same funct

15 However, deeper insight into the JC virus and its pathogenesis and the immune response du

16 drocyte cell line supports both infection by JC virus and robust levels of JCV DNA replication.

17 ecific manner, since T antigen repressed the JC virus and simian virus 40 (SV40) early promoters in g

18 and the other closely related polyomaviruses JC virus and SV40.

19 ls expressed the 5HT2a receptor (5HT2aR) for JC virus and were highly susceptible to infection.

20 with viruses (3 with cytomegalovirus, 2 with JC virus, and 2 with varicella zoster virus) and 3 with

21 infect human beings (simian virus 40 [SV40], JC virus, and BK virus) was associated with non-Hodgkin

22 e, reliable and sensitive PCR testing of the JC virus, and broadened criteria for recognition of PML

23 JC virus antibodies were found in 5 of 13 patients.

24 t demonstrate a 50 to 60% prevalence of anti-JC virus antibodies, a low false-negative rate, and an a

25 Patients who were positive for anti-JC virus antibodies, had taken immunosuppressants before

26 tive or negative status with respect to anti-JC virus antibodies, prior or no prior use of immunosupp

27 actors: positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, an

28 Positive status with respect to anti-JC virus antibodies, prior use of immunosuppressants, an

29 mong the patients who were negative for anti-JC virus antibodies, with the incidence estimated to be

30 before the diagnosis were positive for anti-JC virus antibodies.

31 lytical false-negative rate of a 2-step anti-JC virus antibody assay.

32 m and plasma samples were collected for anti-JC virus antibody detection using an analytically valida

33 S patients switching from natalizumab due to JC virus antibody positivity at 3 Swedish multiple scler

34 patients who switch from natalizumab due to JC virus antibody positivity.

35 TRATIFY-1 will confirm the stability of anti-JC virus antibody prevalence over time.

36 At baseline (n = 1,096), overall anti-JC virus antibody prevalence was 56.0% (95% confidence i

37 ing age and male gender with increasing anti-JC virus antibody prevalence.

38 Blood samples were available for anti-JC virus antibody testing from 5896 patients with multip

39 Many JC virus antibody-positive relapsing-remitting multiple

40 new tools for risk stratification including JC-virus antibody status, prior immunosuppression, and l

41 sly demonstrated that T antigen controls the JC virus basal promoter in a glial cell-specific manner,

42 results suggest that T antigen activates the JC virus basal promoter in nonglial cells by interaction

43 These data demonstrate that JC virus binding to human glial cells induces an intrace

44 Advances in the understanding of JC virus biology have shed new light on the pathogenesis

45 opathy, and advances in the understanding of JC virus biology.

46 Human polyomaviruses (JC virus, BK virus and simian virus 40) are causative ag

47 Additionally, the JC virus can also lead to novel neurological disorders s

48 s been demonstrated that the closely related JC virus can enter cells in clathrin-coated vesicles and

49 Recently, we have demonstrated that JC virus can infect cerebellar granule cell neurons and

50 The JC virus capsid is composed of 72 pentamers of the major

51 ypothesis has gained general acceptance that JC virus causes a primary infection in childhood and ent

52 es, but polymerase chain reaction documented JC virus co-infection in one of five cases so tested.

53 region of the human neurotropic polyomavirus JC virus contains a consensus NF-kappa B site which has

54 It also appeared that archetype JC virus could sporadically be identified in PML patient

55 Urine was collected for JC virus DNA detection.

56 own on magnetic resonance imaging regressed; JC virus DNA in plasma, likely originating from the brai

57 JC virus DNA in the CSF and peripheral blood was quantif

58 JC virus DNA may harbor in CD34+ cells in bone marrow th

59 ng oligodendrocytes, which were positive for JC virus DNA on in situ hybridization.

60 JC virus DNA was detectable within cell compartments of

61 ient brain, although selection of rearranged JC virus DNA was favored.

62 JC virus DNA was not detected in CSF or peripheral blood

63 right hemispheric and brainstem lesions and JC virus DNA was undetectable in his cerebrospinal fluid

64 The JC virus early promoter directs cell-specific expression

65 a cells but induced strong activation of the JC virus early promoter in nonglial cells.

66 ch as JC virus granule cell neuronopathy and JC virus encephalopathy, and might also cause meningitis

67 The late region of the human neurotropic JC virus encodes a 71 amino acid protein, named Agnoprot

68 The late region of human neurotropic JC virus encodes a small 71-amino-acid agnoprotein that

69 are the requirement with the closely related JC virus for an intact actin cytoskeleton during intrace

70 Isolates of the human polyomavirus JC virus from patients with the frequently fatal demyeli

71 on of the primary tumor may have reactivated JC virus gene expression and led to redevelopment of the

72 Neurotropic JC virus generally harbors reorganized noncoding control

73 lead to novel neurological disorders such as JC virus granule cell neuronopathy and JC virus encephal

74 ge T-antigen (T-Ag) of the human neurotropic JC virus, has been shown to modulate the Wnt-signaling p

75 The human polyomavirus, JC virus, has recently been associated with several huma

76 In contrast, urinary JC virus highly resembled the archetype virus, and urine

77 TAT1 plays a critical role in the control of JC virus in the central nervous system.

78 encephalopathy patients are now negative for JC virus in the cerebrospinal fluid by polymerase chain

79 confirmed by brain biopsy or by identifying JC virus in the cerebrospinal fluid by polymerase chain

80 cal diagnosis by use of MRI and detection of JC virus in the CSF was established in all but one case.

81 the recent discovery of the presence of the JC virus in the grey matter invite us to reappraise the

82 hs of natalizumab therapy, the prevalence of JC virus in the urine of the 19 patients increased from

83 ew of the possible causes of reactivation of JC virus in this population has illustrated the need to

84 We detected BK and JC viruses in the urine of 35 and 16% of transplant reci

85 ukoencephalopathy caused by John Cunningham (JC) virus in immunocompromised humans.

86 confirming sequences of SV40 (but not BK or JC virus) in his kidney biopsy and urine by polymerase c

87 tem to control the expression of RB2/p130 in JC virus-induced hamster brain tumor cells to study in v

88 revealed typical features of PML as well as JC virus-infected neurons.

89 ndrocyte progenitor cells are susceptible to JC virus infection and indicates that cells poised to re

90 hese results indicate that susceptibility to JC virus infection occurs at the molecular level and als

91 anagement of IRIS associated with PML due to JC virus infection remains the most challenging, as no a

92 HLA-A*02 persons in response to either BK or JC virus infection.

93 and increases in peripheral CD4+ T cells and JC virus intrathecal antibodies were observed.

94 JC virus is activated to replicate in glial cells of man

95 iological agent of PML, the polyomavirus JC (JC virus), is ubiquitous within the human population.

96 However, T antigen containing the JC virus J domain was functional in these assays, althou

97 e archetype strain of the human polyomavirus JC virus (JCV(Cy)), unlike its neurotropic counterpart (

98 omegalovirus (CMV) was assayed in urine, and JC virus (JCV) and BK virus (BKV) DNAs were assayed in u

99 of the closely related human polyomaviruses JC virus (JCV) and BK virus (BKV) in mesothelioma remain

100 For the human polyomaviruses JC virus (JCV) and BK virus (BKV), the first step to a s

101 of CNS infection, as many viruses, including JC virus (JCV) and HIV, cannot replicate in rodent cells

102 Agnoprotein is a small regulatory protein of JC virus (JCV) and is required for the successful comple

103 detected in all patients, notably including JC virus (JCV) and Torque teno virus (TTV) and interesti

104 undertaken to define the prevalence of anti-JC virus (JCV) antibodies in multiple sclerosis (MS) pat

105 ment is associated with the presence of anti-JC virus (JCV) antibodies.

106 A 55-year-old, JC virus (JCV) antibody-positive patient with multiple s

107 JC virus (JCV) causes progressive multifocal leukoenceph

108 ous system, with the human neurotropic virus JC virus (JCV) causes the fatal demyelinating disease pr

109 otide resolution and relative copy number of JC virus (JCV) clinical standards.

110 determine the clinical utility of measuring JC virus (JCV) DNA in blood or urine of natalizumab-trea

111 The detection and semiquantitation of JC virus (JCV) DNA in cerebrospinal fluid (CSF) is progn

112 JC virus (JCV) DNA in the cerebrospinal fluid (CSF) prov

113 reas transplant patients, BK virus (BKV) and JC virus (JCV) DNAemia were observed most commonly in ki

114 The human neurotropic JC virus (JCV) genome encodes an auxiliary protein calle

115 We sought to determine the prevalence of JC virus (JCV) in bone marrow samples from human immunod

116 ML), a fatal demyelinating disease caused by JC virus (JCV) infection of oligodendrocytes, may develo

117 natalizumab-treated MS patients is linked to JC virus (JCV) infection.

118 The human polyomavirus JC virus (JCV) infects 70% of the population worldwide.

119 The human polyomavirus JC virus (JCV) infects myelin-producing cells in the cen

120 Infectious entry of JC virus (JCV) into human glial cells occurs by receptor

121 Human polyomavirus JC virus (JCV) is a causative agent of progressive multi

122 JC virus (JCV) is a common human polyomavirus that infec

123 JC virus (JCV) is a human polyomavirus and the causative

124 JC virus (JCV) is a neurotropic polyomavirus infecting g

125 JC virus (JCV) is a polyoma virus that commonly infects

126 JC virus (JCV) is a polyomavirus that ubiquitously infec

127 ts have indicated that the human neurotropic JC virus (JCV) is able to induce cerebellar neoplasms in

128 JC virus (JCV) is latent in the kidneys and lymphoid org

129 cation of the human neurotropic polyomavirus JC virus (JCV) is regulated by cell membrane receptors a

130 The human polyomavirus JC virus (JCV) is the causative agent of the fatal demye

131 The human polyomavirus JC virus (JCV) is the etiologic agent of a fatal central

132 JC virus (JCV) is the etiologic agent of progressive mul

133 The human polyomavirus JC virus (JCV) is the etiologic agent of the fatal demye

134 ur and other laboratories indicated that the JC virus (JCV) late regulatory protein, agnoprotein, pla

135 Infection with JC virus (JCV) may lead to development of demyelinating

136 It has been suggested that JC virus (JCV) might travel to the central nervous syste

137 A comparison of antibody titers to JC virus (JCV) or BK virus (BKV) was made by hemagglutin

138 e diagnosed either using cerebrospinal fluid JC virus (JCV) polymerase chain reaction, brain biopsy,

139 Cell-type-specific transcription of the JC virus (JCV) promoter in glial cells initiates a serie

140 d c-Fos in transcriptional regulation of the JC virus (JCV) promoter in glial cells.

141 Rearrangements of the JC virus (JCV) regulatory region (RR) are consistently f

142 opathy in kidney allograft recipients, while JC virus (JCV) replication occurs in the glial cells of

143 JC virus (JCV) seropositivity is a risk factor for progr

144 To examine the mode of JC virus (JCV) transmission, we collected urine samples

145 JC virus (JCV) viruria is more common than BK virus (BKV

146 de corresponding to the previously described JC virus (JCV) VP1 homolog sequence ILMWEAVTL (JCV VP1p1

147 rt and trafficking of the human polyomavirus JC virus (JCV) with that of simian virus 40 (SV40).

148 disease-causing members (BK virus (BKV) and JC virus (JCV)) identified.

149 for human polyomaviruses: 9 with BKV, 9 with JC virus (JCV), 1 with SV40, and 1 with both JCV and SV4

150 JC virus (JCV), a human neurotropic polyomavirus, demons

151 JC virus (JCV), a human polyomavirus, exhibits oncogenic

152 JC virus (JCV), a human polyomavirus, has been found in

153 JC virus (JCV), a member of the polyomavirus family, cau

154 JC virus (JCV), along with other members of the polyomav

155 Samples were analyzed for BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) by convention

156 Samples were analyzed for BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) using convent

157 d region in the large T antigen gene of BKV, JC virus (JCV), and simian virus 40 (SV40).

158 t three types of polyomavirus infect humans: JC virus (JCV), BK virus (BKV) and Simian Vacuolating vi

159 tifocal leukoencephalopathy (PML), caused by JC virus (JCV), can occur in patients receiving natalizu

160 The human polyomavirus, JC virus (JCV), encodes two regulatory proteins at the e

161 tional regulation of the human polyomavirus, JC virus (JCV), genome.

162 ection of the ubiquitous human polyomavirus, JC virus (JCV), in samples derived from several types of

163 iruses, including Simian Virus 40 (SV40) and JC virus (JCV), is a multifunctional phosphoprotein that

164 on of glial cells by the human polyomavirus, JC virus (JCV), leads to a rapidly progressing and unifo

165 JC virus (JCV), the causative agent of progressive multi

166 JC virus (JCV), the causative agent of the fatal human d

167 pathogen-specific primers to detect DNA from JC virus (JCV), varicella zoster virus (VZV), cytomegalo

168 n paid to human polyomaviruses, particularly JC virus (JCV), which infects greater than 80% of the hu

169 ncomitant presence of the human papovavirus, JC virus (JCV), which is the etiologic agent of the suba

170 to 80% of humans express serum antibodies to JC virus (JCV), yet considerably fewer people develop PM

171 is the most common clinical presentation of JC virus (JCV)-associated central nervous system (CNS) d

172 linked immunosorbent assay (ELISA) to detect JC virus (JCV)-specific antibodies in multiple sclerosis

173 JC virus (JCV)-specific CD8+ cytotoxic T lymphocytes (CT

174 JC virus (JCV)-specific cytotoxic T lymphocytes (CTL) in

175 tion of glial cells by the human neurotropic JC virus (JCV).

176 endrocytes by the opportunistic polyomavirus JC virus (JCV).

177 an genotypes (Types 2 and 7) and subtypes of JC virus (JCV).

178 ation of the human neurotropic polyomavirus, JC virus (JCV).

179 eactivation of BK virus (BKV) or more rarely JC virus (JCV).

180 s and replication of some viruses, including JC virus (JCV).

181 an immunodeficiency virus type I (HIV-1) and JC virus (JCV).

182 ral nervous system, by the human neurotropic JC virus (JCV).

183 omoters of the ubiquitous human polyomavirus JC virus (JCV).

184 s of human polyomaviruses BK virus (BKV) and JC virus (JCV).

185 gered by infection with the human gliotropic JC virus (JCV).

186 ised individuals are infected with the human JC virus (JCV).

187 for sustaining the productive replication of JC virus (JCV).

188 al disease caused by the reactivation of the JC virus (JCV).

189 demyelinating disease of the brain caused by JC virus (JCV).

190 e DNA recombination between polyomavirus JC (JC virus [JCV]) and Epstein-Barr virus (EBV) at sequence

191 n between large T antigen and Rb proteins in JC virus-mediated oncogenesis.

192 n immunosuppressed macaques, which parallels JC virus-neuronal infection in immunosuppressed patients

193 may be an important aspect of both SV40 and JC virus neuropathogenesis in their respective hosts.

194 Subclinical reactivation of JC virus occurs frequently in natalizumab-treated patien

195 chain-reaction assays in blood and urine for JC virus reactivation; BK virus, a JC virus-related poly

196 In addition, we have determined that JC virus readily infects G144 cells.

197 JC virus regulatory-region sequences in blood samples an

198 zyme-linked immunosorbent assay and analyzed JC virus regulatory-region sequences.

199 urine for JC virus reactivation; BK virus, a JC virus-related polyomavirus, was used as a control.

200 nd its recurrence for their association with JC virus revealed that, while the viral genome is presen

201 different rearrangements were present in the JC virus sequences present in the WHO standard across mu

202 uppressive agents (n = 8), and reported anti-JC virus seropositivity (n = 13).

203 strong cellular immune response mediated by JC virus-specific CD8 cytotoxic T lymphocytes, which are

204 The JC virus-specific cellular immune response dropped signi

205 g is associated with a transient drop in the JC virus-specific cellular immune response.

206 We determined JC virus-specific T-cell responses by means of an enzyme

207 JC virus susceptibility correlated with significantly hi

208 s were not cross-reactive on the human BK or JC virus T ags.

209 n, 18q LOH was independently associated with JC virus T antigen (odds ratio [OR] = 1.93; P = .0077),

210 The IRS-1 domain responsible for a direct JC virus T-antigen binding was localized within the N-te

211 nt of IRS-1 inhibited growth and survival of JC virus T-antigen-transformed cells in anchorage-indepe

212 pe, LINE-1 methylation, and John Cunningham (JC) virus T antigen.

213 endrocyte progenitor cells to infection with JC virus, the causative agent of progressive multifocal

214 Most adults who are infected with the JC virus, the etiologic agent in PML, do not have sympto

215 protein activates the major late promoter of JC virus through a Tat-responsive DNA element, termed up

216 ogy, representing the immune response to the JC virus to a variable extend.

217 Simian virus 40 and JC virus, two closely related members of the polyomaviru

218 d large T antigen expression by BK virus and JC virus, two important, pathogenic human polyomaviruses

219 for both murine polyomavirus and SV40, while JC virus uses serotonin receptors.

220 After 18 months of treatment, JC virus was detectable in 3 of 15 available plasma samp

221 ncephalopathy or evidence of reactivation of JC virus were identified.

222 of SV40 VLPs but not by VLPs for BK virus or JC virus, which are related human polyomaviruses) was in

223 isease that results from reactivation of the JC virus, which generally occurs in immunosuppressed hos

224 tter of the brain caused by the polyomavirus JC virus, which typically occurs only in immunocompromis