ライフサイエンスコーパス: GBV-C

1 GBV-C E2 expression significantly inhibited IL-2 release

2 GBV-C E2 protein and a synthetic peptide representing th

3 GBV-C E2 protein inhibits HIV-1 entry, and an antigenic

4 GBV-C genotype 1 and 5 isolates replicated in lymphocyte

5 GBV-C has a protective effect, in part through a competi

6 GBV-C infection and expression of the GBV-C nonstructura

7 GBV-C infection has not been convincingly associated wit

8 GBV-C infection is associated with reduced T cell activa

9 GBV-C infection is common in people with HIV infection a

10 GBV-C infection may play an etiologic role in a small pr

11 GBV-C infection modestly alters T cell homeostasis in vi

12 GBV-C infection was detected in 85 percent of men with H

13 GBV-C is a lymphotropic virus capable of persistent infe

14 GBV-C is associated with lower human immunodeficiency vi

15 GBV-C is related to hepatitis C virus but does not appea

16 GBV-C load correlated with DNTC percentage (P = .004).

17 GBV-C NS5A protein from an isolate that was cleared by I

18 GBV-C replicates in peripheral blood mononuclear cells (

19 GBV-C RNA never reappeared once it was cleared, and ther

20 GBV-C RNA positivity was associated with NHL overall [OR

21 GBV-C RNA was detected </=120 days following the first t

22 GBV-C RNA was detected at all visits in 32, was never de

23 GBV-C RNA was present in 5 of 22 (23%) anti-HCV-positive

24 GBV-C status 12 to 18 months after HIV seroconversion wa

25 GBV-C viremia is associated with lower mortality, and GB

26 GBV-C viremia was significantly associated with prolonge

27 GBV-C-induced modulation in T-cell cytokines may contrib

28 GBV-C-infected patients exhibited a complete virological

29 GBV-C-viremic subjects had significantly reduced CD4(+)

30 GBV-C/HGV infection also had no significant impact on th

31 GBV-C/HGV infection was not related to the number of blo

32 GBV-C/HGV RNA was commonly detected in post-LT patients

33 Organs from four GBVC-positive donors and 47 GBV-C-negative donors procured by the New England Organ

34 neys from GBV-C RNA-positive donors acquired GBV-C RNA after transplantation, compared with 4 of 40 (

35 Only one man acquired GBV-C viremia between the early and the late visit, but

36 We estimated the risk of acquiring GBV-C RNA and predictors of GBV-C acquisition, using poo

37 rted in HIV-positive individuals with active GBV-C coinfection.

38 Few studies describe predictors of acute GBV-C infection following transfusion in HIV-infected pa

39 Thus, African GBV-C genotypes can inhibit HIV replication in vitro.

40 n various cell subsets in the 3 months after GBV-C detection.

41 cytokines and chemokines were reduced after GBV-C detection, including many proinflammatory cytokine

42 tested for GBV-C RNA and antibodies against GBV-C E2 protein, and responses to HAART were evaluated.

43 All GBV-C E2 Abs neutralized diverse isolates of HIV-1 with

44 Although GBV-C could be transmitted by organ transplantation, the

45 Although GBV-C is associated with acute posttransfusion hepatitis

46 d a significant reduction in mortality among GBV-C coinfected VATS subjects, after adjusting for HAAR

47 The data indicate that GBV-A and GBV-C are unique members of the Flaviviridae that do not

48 es, including the highly divergent GBV-A and GBV-C viruses, are functionally similar to HCV.

49 GB viruses A and C (GBV-A and GBV-C) are two recently described RNA viruses which appe

50 ternal ribosome entry site in both GBV-A and GBV-C.

51 sites of polyprotein initiation in GBV-A and GBV-C.

52 y from 30 patients positive for both HIV and GBV-C (hereafter, "cases") and 30 patients positive for

53 rus associated with hepatitis in humans, and GBV-C/HGV coinfection is common in patients chronically

54 emia is associated with lower mortality, and GBV-C acquisition via transfusion is associated with a s

55 Both survival and GBV-C status were associated with age, with older patien

56 HIV-1 replication in vivo and in vitro, and GBV-C coinfection is associated with prolonged survival

57 Anti-GBV-C is highly associated with viral clearance and prot

58 Anti-GBV-C was detected in all 8 instances of RNA clearance.

59 e were no new GBV-C infections among 61 anti-GBV-C-positive IDUs observed for 382 person-years, thoug

60 The odds of detecting anti-GBV-C were 103-fold higher in participants without detec

61 Rabbit anti-GBV-C E2 Abs neutralized HIV-1-pseudotyped retrovirus pa

62 odds ratios (OR) for the association between GBV-C and NHL overall and NHL subtypes.

63 were used to examine the association between GBV-C coinfection and mortality in the VATS cohort.

64 le conclusions about the association between GBV-C infection and clinical outcomes.

65 into the epidemiological association between GBV-C infection and longer survival in HIV-infected indi

66 nced the significance of association between GBV-C viremia and response to antiretroviral therapy.

67 allow identification of differences between GBV-C and hepatitis C virus cultivation in vitro.

68 The inability to distinguish between GBV-C variants by using small segments of coding sequenc

69 indicates that an association exists between GBV-C infection and response to HAART.

70 anding the mechanisms of interaction between GBV-C and HIV may provide insight into the progression o

71 he possibility of structural mimicry between GBV-C E2 protein and HIV-1 particles.

72 direction of any causal relationship between GBV-C infection and HIV disease markers in the context o

73 Subjects with both GBV-C E2 antibody and viremia had significantly lower GB

74 res of peripheral-blood mononuclear cells by GBV-C coinfection.

75 Of 6 blood recipients infected by GBV-C RNA-positive donors, 4 (67%) became anti-E2 positi

76 ects (13.3%), all of whom tested negative by GBV-C reverse-transcription polymerase chain reaction (R

77 ings shed light on a novel mechanism used by GBV-C E2 to inhibit HIV-1 replication and may provide in

78 Persistent GB virus type C (GBV-C) infection is associated with survival and a serum

79 GB virus type C (GBV-C) is a human flavivirus that may cause persistent i

80 GB virus type C (GBV-C) is a single-stranded positive-sense RNA virus cla

81 GB virus type C (GBV-C) is an apparently nonpathogenic virus that replica

82 Persistent infection with GB virus type C (GBV-C) is associated with prolonged survival in HIV-1-in

83 GB virus type C (GBV-C) is transmitted by sexual or parenteral exposure a

84 GB virus type C (GBV-C) viremia is associated with reduced CD4+ T cell ex

85 ople (dengue virus (DV) and GB virus type C (GBV-C)).

86 GB virus C (GBV-C or hepatitis G virus) is a recently described flav

87 Phylogenetic analysis of 44 GB virus C (GBV-C) 5'-untranslated region (5'-UTR) sequences from 37

88 The virus is closely related to GB virus C (GBV-C) and distantly related to hepatitis C virus, GBV-A

89 An association between GB virus C (GBV-C) and improved outcomes of human immunodeficiency v

90 To study how GB virus C (GBV-C) coinfection affects the response to highly active

91 d People coinfected with HIV and GB virus C (GBV-C) have lower mortality than HIV-positive individual

92 GB virus C (GBV-C) infection is associated with reduced T-cell activ

93 GB virus C (GBV-C) infection is common in humans and may persist for

94 GB virus C (GBV-C) infection is transmitted by blood exposure and as

95 GB virus C (GBV-C) is a common, apparently nonpathogenic human flavi

96 GB virus C (GBV-C) is a lymphotropic human virus discovered in 1995

97 vered hepatitis G virus (HGV) or GB virus C (GBV-C) is widely distributed in human populations, and h

98 GB virus C (GBV-C) RNA and envelope antibody were assessed in a medi

99 us (HGV), were tested for HGV or GB virus C (GBV-C) RNA.

100 Upon coinfection, GB virus C (GBV-C) suppresses HIV-1 replication in vivo and in vitro

101 d for detection of antibodies to GB virus C (GBV-C) using a recombinant E2 protein expressed in CHO c

102 individuals were coinfected with GB virus C (GBV-C), a parenterally transmitted virus.

103 lly transmitted hepatitis virus, GB virus C (GBV-C), has opened avenues to study the prevalence and r

104 GB virus C (GBV-C), which is not known to be pathogenic in humans, r

105 h the immunomodulatory pegivirus GB virus C (GBV-C).

106 nfection who are coinfected with GB virus C (GBV-C, or hepatitis G virus) have delayed progression of

107 GB virus C (GBV-C; also called hepatitis G virus) is a common cause

108 sociation between infection with GB virus-C (GBV-C) and non-Hodgkin lymphoma (NHL).

109 of yet another hepatitis virus, GB virus-C (GBV-C), has provided the opportunity to study the preval

110 e other human pegivirus, HPgV-1 (GB virus C [GBV-C]).

111 DNA from the plasma of a person with chronic GBV-C viremia.

112 ore often than patients without [correction] GBV-C and had a greater increase in median CD4 cell coun

113 There are 5 distinct GBV-C genotypes localized to specific geographic regions

114 -UTR sequences from 129 globally distributed GBV-C isolates and sequences from the second envelope pr

115 Among ELISA1-positive donors, GBV-C RNA was present in 13 of 35 (37%) donors with HCV

116 titis virus type G envelope, HIV-1 envelope, GBV-C envelope, or no viral envelope.

117 Findings GBV-C infection of peripheral-blood mononuclear cells re

118 CV, using a second-generation ELISA, and for GBV-C RNA by reverse transcription PCR.

119 to study the prevalence and risk factors for GBV-C infection among patients undergoing renal transpla

120 0 patients positive for HIV and negative for GBV-C (hereafter, "controls").

121 of the 218 patients who tested negative for GBV-C RNA (56.4 percent; P<0.001).

122 V ELISA1-positive donors tested positive for GBV-C RNA compared with 6 of 82 (7.3%) ELISA1-negative d

123 d Immunodeficiency Syndrome Cohort Study for GBV-C viremia (by means of a reverse-transcriptase-polym

124 od samples from 489 subjects were tested for GBV-C markers in pretransfusion and posttransfusion samp

125 od samples from 489 subjects were tested for GBV-C markers.

126 iagnostic PLCO serum samples were tested for GBV-C RNA (as a measure of active infection) and E2 anti

127 irus (HIV)-infected patients were tested for GBV-C RNA and antibodies against GBV-C E2 protein, and r

128 tis C virus (HCV) infection, were tested for GBV-C RNA by polymerase chain reaction using degenerate

129 ith 4 of 40 (10%) recipients of kidneys from GBV-C RNA-negative donors.

130 ne of three (33%) recipients of kidneys from GBV-C RNA-positive donors acquired GBV-C RNA after trans

131 Extracellular microvesicles from GBV-C E2-expressing cells contained E2 protein and inhib

132 of GBV-C RNA among recipients of organs from GBV-C RNA-positive and -negative donors, were studied at

133 different between recipients of organs from GBV-C RNA-positive and -negative donors.

134 Among recipients of organs from GBV-C RNA.

135 Infectious RNA transcripts from GBV-C cDNA should prove useful for studying viral replic

136 e data demonstrate that RNA transcripts from GBV-C full-length cDNA are infectious in primary CD4-pos

137 Expression of glycosylated GBV-C E2 inhibited HIV-1 Gag precursor processing, resul

138 IV-infected patients, 144 (39.8 percent) had GBV-C viremia in two tests.

139 eveloped to detect covariant sites among HGV/GBV-C sequences of different genotypes.

140 with the high rate of sequence change of HGV/GBV-C over short observation periods.

141 (8,500 bases) of different genotypes of HGV/GBV-C showed an excess of invariant synonymous sites (at

142 nd long-term rates of sequence change of HGV/GBV-C violates the assumptions of the "molecular clock."

143 correlation between negative, low, and high GBV-C RNA levels and increasing reduction in HIV RNA fol

144 We identified GBV-C RNA in purified CD4(+) and CD8(+) T lymphocytes an

145 We identified GBV-C virus isolates representing genotypes 1, 2, and 5

146 nes into culture supernatants were higher in GBV-C-infected cells than in mock-infected cells.

147 xpression of CCR5 was significantly lower in GBV-C-infected cells than in mock-infected cells.

148 ion in chronic immune activation observed in GBV-C/HIV-coinfected individuals.

149 ngs provide the first evidence that incident GBV-C infection alters mortality in HIV-infected patient

150 y occurring human and experimentally induced GBV-C E2 Abs were examined for their ability to neutrali

151 Interpretation GBV-C induces HIV-inhibitory chemokines and reduces expr

152 virin therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and quantitated in serum samp

153 antibody and viremia had significantly lower GBV-C RNA levels than did viremic subjects without E2 an

154 To determine the optimal method of measuring GBV-C RNA in clinical samples, samples obtained from 939

155 or expression of CD4 contained 100-fold-more GBV-C RNA than CD4-negative cells.

156 C virus and human pegivirus (formerly named GBV-C) interfere with T-cell receptor (TCR) signaling by

157 d once it was cleared, and there were no new GBV-C infections among 61 anti-GBV-C-positive IDUs obser

158 patients survived; in contrast, only 22% of GBV-C(-) patients survived.

159 ll counts than controls after acquisition of GBV-C infection.

160 Acquisition of GBV-C RNA (n = 39) was associated with lower mortality i

161 been proposed as the reason for clearance of GBV-C among persons positive for human immunodeficiency

162 visit, but 9 percent of men had clearance of GBV-C RNA between these visits.

163 udies demonstrate that accurate detection of GBV-C RNA by nested RT-PCR requires the use of primers r

164 s may contribute to the beneficial effect of GBV-C in HIV-infected individuals.

165 esting an overall antiinflammatory effect of GBV-C in HIV-positive subjects.

166 The inhibitory effect of GBV-C on HIV replication was blocked by incubation with

167 emonstrate an anti-HIV replication effect of GBV-C.

168 tanding the separate and combined effects of GBV-C and age on Ebola virus survival may lead to new tr

169 Furthermore, the effects of GBV-C on IL-2 and IL-2-signaling pathways may contribute

170 this study, we showed that the expression of GBV-C E2 inhibited HIV-1 Gag assembly and release.

171 Furthermore, expression of GBV-C NS5A protein in a CD4(+) cell line resulted in upr

172 or the existence of the four major groups of GBV-C isolates previously described, although phylogenet

173 Thus, the groups of GBV-C variants previously identified upon analysis of th

174 region sequences does not identify groups of GBV-C variants that correlate with geographic origin.

175 To determine the clinical impact of GBV-C/HGV infection in such patients and the effect of i

176 st prognosis was associated with the loss of GBV-C RNA (relative hazard for death as compared with me

177 but not at 12 to 18 months, and the loss of GBV-C RNA by 5 to 6 years after HIV seroconversion was a

178 A marker of GBV-C infection was detected in 110 (94.8%) of 116 IDUs.

179 ignificantly underestimate the occurrence of GBV-C infection.

180 isk of acquiring GBV-C RNA and predictors of GBV-C acquisition, using pooled logistic regression.

181 rom 37 individuals suggested the presence of GBV-C genotypes that correlated with geographic origin:

182 y Vietnamese were tested for the presence of GBV-C/HGV RNA by the reverse transcription polymerase ch

183 splantation clinical data, and prevalence of GBV-C RNA among recipients of organs from GBV-C RNA-posi

184 The prevalence of GBV-C RNA, extrapolated to all cadaver organ donors, was

185 The prevalences of GBV-C viremia vary widely in different studies, and ther

186 sm(s) of HIV inhibition, the NS5 proteins of GBV-C, DV, hepatitis C virus, West Nile virus, and yello

187 (21 to 45 years) having the highest rate of GBV-C infection.

188 s compared with 28 and 10%, respectively, of GBV-C RNA-negative recipients.

189 was observed in 35 and 18%, respectively, of GBV-C RNA-positive recipients compared with 28 and 10%,

190 ion is associated with a significant risk of GBV-C acquisition among HIV-infected patients.

191 The risk of GBV-C RNA acquisition increased with each unit transfuse

192 mechanisms underlying the protective role of GBV-C in HIV-infected patients.

193 he epidemiology and clinical significance of GBV-C.

194 Transmission of GBV-C by blood transfusion was inversely related to HIV

195 red to determine the risk of transmission of GBV-C by organ transplantation and its role in posttrans

196 In addition, two types of GBV-C particles were identified in cell lysates; these p

197 ed to topologically map immunogenic sites on GBV-C E2 and for the ability to detect or block recombin

198 istronic RNAs containing 5' ends of GBV-A or GBV-C fused in-frame with the chloramphenicol acetyltran

199 5 positive patients were positive for HGV or GBV-C by the commercial RT-PCR assay.

200 mmercially available RT-PCR assay for HGV or GBV-C gave concordant results for 96% of the patients te

201 hemodialysis patients were tested for HGV or GBV-C RNA, 25 patients (26%) were positive by the RT-nes

202 but two positive patients had unique HGV or GBV-C sequences.

203 Hepatitis G virus (HGV or GBV-C) is a newly discovered human flavivirus distantly

204 ol for differences in the duration of HIV or GBV-C infection.

205 the presence of E2 antibody (46 percent) or GBV-C RNA (39 percent).

206 ment among different laboratories performing GBV-C RNA detection in quality control studies.

207 dies found an association between persistent GBV-C infection and improved survival in HIV-positive in

208 r death as compared with men with persistent GBV-C RNA, 5.87; P=0.003).

209 imes as likely to die as men with persistent GBV-C viremia (95 percent confidence interval, 1.34 to 5

210 Pretransplantation GBV-C RNA was present in 18 of 99 (18%, 95% confidence i

211 ved among recipients with pretransplantation GBV-C infection, the analyses presented here do not allo

212 rates that longer coding regions can produce GBV-C groupings that are similar to that determined from

213 Using a quantitative GBV-C RNA method, the GBV-C RNA concentration did not co

214 Rabbit GBV-C E2 Abs inhibited HIV attachment to cells but did n

215 Addition of purified recombinant GBV-C E2 protein to primary human CD4+ and CD8+ T cells

216 ncentrations of positive- and negative-sense GBV-C RNA over time, and the detection of the GBV-C E2 a

217 A assay: 10 patients were positive for serum GBV-C/HGV RNA.

218 ked but usually transient reduction in serum GBV-C/HGV RNA, and ribavirin had, at most, a modest anti

219 erferon-alpha and ribavirin therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and qua

220 We demonstrate that serum GBV-C particles inhibited activation of primary human T

221 We studied GBV-C NS5A to determine whether it is involved in inhibi

222 To study GBV-C E2 antigenicity and cell binding, murine anti-E2 m

223 iral therapy were associated with subsequent GBV-C RNA acquisition, after control for units of blood

224 anti-peptide Abs raised against a synthetic GBV-C E2 peptide.

225 We conclude that GBV-C/HGV infection is very common in LT recipients, but

226 Our study demonstrates that GBV-C infection precedes development of NHL.

227 We found that GBV-C infection increased gene expression of Th1 cytokin

228 ex vivo from infected donors and found that GBV-C replicated in vitro in these PBMC subsets, suggest

229 vitro in these PBMC subsets, suggesting that GBV-C is a panlymphotropic virus.

230 This suggests that GBV-C and TTV may have different routes of transmission.

231 The GBV-C envelope glycoprotein E2 has been reported to inte

232 The GBV-C nonstructural phosphoprotein (NS5A) is predicted t

233 ation in tet-off Jurkat cells expressing the GBV-C envelope glycoprotein (E2) following activation th

234 Using a quantitative GBV-C RNA method, the GBV-C RNA concentration did not correlate with baseline

235 BV-C RNA over time, and the detection of the GBV-C E2 antigen by confocal microscopy.

236 ng three additional conserved regions of the GBV-C genome (the 5' nontranslated region and the nonstr

237 hods amplifying four separate regions of the GBV-C genome.

238 helicase and 5'-untranslated regions of the GBV-C genome.

239 on was related to the dose and timing of the GBV-C infection.

240 GBV-C infection and expression of the GBV-C nonstructural protein 5A (NS5A) and the DV NS5 pro

241 ght N-terminal residues, suggesting that the GBV-C E2 protein contains a single immunodominant antige

242 Taken together, these data indicate that the GBV-C E2 protein has a structural motif that elicits Abs

243 These data provide evidence that the GBV-C E2 protein may contribute to the block in CD4+ T c

244 egments of coding sequence suggests that the GBV-C genome is constrained.

245 Both of these GBV-C NS5A proteins were expressed in a CD4+ T cell line

246 Fifty-three percent of these GBV-C(+) patients survived; in contrast, only 22% of GBV

247 d with full-length RNA transcripts from this GBV-C clone resulted in viral replication.

248 Thus, GBV-C infection is associated with an increase in DNTCs,

249 Thus, GBV-C NS5A protein alters the cellular milieu necessary

250 Thus, GBV-C reduced global T cell activation via competition b

251 without HIV-1 viremia, the presence of Ab to GBV-C glycoprotein E2 is also associated with survival.

252 prevalence of GB virus-C/hepatitis G virus (GBV-C/HGV) infection in liver transplant recipients tran

253 GB virus C/hepatitis G virus (GBV-C/HGV) is a newly described virus associated with he

254 GB virus C or hepatitis G virus (GBV-C/HGV), a novel Flavivirus, is detected in 1.5% of U

255 cases (1.8%) and seven controls (0.5%) were GBV-C RNA-positive.

256 ith lower mortality in 294 subjects who were GBV-C negative at baseline, adjusting for baseline covar

257 fusion in 22 (7.5%) of 294 subjects who were GBV-C negative before transfusion.

258 ected with both viruses to determine whether GBV-C infection alters replication in vitro.

259 r studies are necessary to establish whether GBV-C may have deleterious effects on the host at the ce

260 isting data on potential mechanisms by which GBV-C interferes with HIV, and the research needed to ca

261 The mechanism(s) by which GBV-C might alter T cell activation or IL-2 signaling ha

262 and younger age (OR=0.97/year, P=0.06) with GBV-C infection.

263 laboratory characteristics, associated with GBV-C infection among cadaver organ donors and recipient

264 P=0.001) were significantly associated with GBV-C infection.

265 of transfused units was not associated with GBV-C transmission.

266 blood mononuclear cells or CD4+ T cells with GBV-C and HIV in vitro results in significantly reduced

267 blood mononuclear cells were coinfected with GBV-C and HIV, and HIV replication was monitored by meas

268 Persistent coinfection with GBV-C is associated with lower human immunodeficiency vi

269 ted individuals, persistent coinfection with GBV-C is associated with prolonged survival, and infecti

270 We examined the effect of coinfection with GBV-C on the survival of patients with HIV infection.

271 as noted among several persons infected with GBV-C RNA-positive blood through transfusion.

272 higher than that among the 144 patients with GBV-C coinfection (relative risk, 3.7; 95 percent confid

273 Forty-one of the patients with GBV-C viremia (28.5 percent) died during the follow-up p

274 and histologic features of the patients with GBV-C/HGV-HCV coinfection compared with those with HCV i

275 antation liver disease among recipients with GBV-C RNA before transplantation was 1.37 (95% CI, 0.55

276 tion blood transfusion among recipients with GBV-C RNA before transplantation was significantly highe

277 tality than HIV-positive individuals without GBV-C infection.

278 sociated with survival; however, men without GBV-C RNA 5 to 6 years after HIV seroconversion were 2.7

279 among the 218 HIV-infected patients without GBV-C coinfection was significantly higher than that amo

280 icantly higher than among recipients without GBV-C RNA (10 versus 7, P = 0.05).