ライフサイエンスコーパス: HGV

1 HGV clearance occurs after many acute infections but unc

2 HGV did not worsen the course of concurrent HCV infectio

3 HGV had little impact on alanine aminotransferase, aspar

4 HGV infection appears to be extremely common in these pa

5 HGV infection does not appear to have a role in mixed cr

6 HGV infection is not associated with hepatic inflammatio

7 HGV infection was present before transplantation in 13%

8 HGV RNA and anti-E2 were mutually exclusive except in 9

9 HGV RNA is not causally related to non-A-E fulminant hep

10 HGV RNA levels are suppressed by IFN but not by zidovudi

11 HGV RNA levels were measured by branched DNA signal ampl

12 HGV RNA levels were not correlated with the severity of

13 HGV RNA was also measured before and after liver transpl

14 HGV RNA was detected at the most recent visit in 38 (15.

15 HGV RNA was detected by polymerase chain reaction (PCR)

16 HGV RNA was detected by reverse transcription polymerase

17 HGV RNA was detected in 30 (17.3%) plasma units, 2 of wh

18 HGV RNA was detected in 4 of 45 patients with a diagnosi

19 HGV RNA was detected in 9 (31%) of 29 short-term IDUs, a

20 HGV RNA was measured using a research-based branched DNA

21 HGV RNA was present in 1 of 28 patients with non-A-E hep

22 HGV RNA-positive patients (HGV-infected and HGV-hepatiti

23 HGV was associated with acute and chronic hepatitis.

24 HGV was common in a group of volunteer blood donors, and

25 HGV was detected by reverse transcriptase-polymerase cha

26 HGV was detected in 29 of 60 (48%) patients.

27 HGV was present in serum of 14 of the 36 patients (38.8%

28 HGV-positive IDUs were younger and had fewer years of dr

29 HGV-RNA was absent from all 20 liver specimens, includin

30 3) HGV RNA becomes undetectable in about one third of recip

31 There were 35 HGV infections among the 357 transfusion recipients; onl

32 All 6 HGV-infected patients were negative for the presence of

33 Compared with HGV-negative patients, the 60 HGV-positive patients (46%), including 22 who were posit

34 For 31 (82%), HGV RNA was also found at all prior visits occurring a m

35 of 29 short-term IDUs, and 5 (56%) of the 9 HGV infections cleared.

36 s in which a transfusion recipient had acute HGV infection after transfusion and samples from all don

37 d; of the remaining 13 patients, 3 had acute HGV infection, and 10 were infected with unidentified ag

38 Although HGV coinfection is frequent in patients with end-stage H

39 Although HGV RNA was demonstrable in the majority (67%) of patien

40 Although HGV RNA was significantly associated with hepatitis C, p

41 serum levels of liver-related enzymes among HGV RNA-positive and -negative participants (P > .20).

42 as developed to detect covariant sites among HGV/GBV-C sequences of different genotypes.

43 ervations indicate that a larger study of an HGV population is required to more clearly define the re

44 ; the levels of alanine aminotransferase and HGV RNA were not well correlated.

45 percent) and those with both hepatitis C and HGV infection (61 percent).

46 7 percent of those with both hepatitis C and HGV infection.

47 eron response was similar in both groups and HGV was not associated with outcome following therapy.

48 ers from the 5' non-coding region of HCV and HGV by a nested polymerase chain reaction (PCR).

49 arly define the relationship between HCV and HGV coinfection and their response to antiviral therapy.

50 The combined HCV and HGV infections were no more severe than HCV infections a

51 Serum HCV and HGV RNA were detected by reverse transcription-polymeras

52 Serum samples were tested for HCV and HGV RNA; HCV RNA was quantitated by branched DNA assay,

53 In coinfected sera, HCV and HGV were quantitated by competitive RT-PCR assays.

54 HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected) developed light-

55 rvival were similar between HGV-positive and HGV-negative patients.

56 in human populations, and homologues such as HGV/GBV-CCPZ and GBV-A are found in a variety of differe

57 nths, only 5% treated with zidovudine became HGV RNA negative, compared with 95% who received IFN-alp

58 ins the reported lack of association between HGV infection and liver pathology encountered in many cl

59 No association between HGV RNA positivity and HCC risk was observed in either H

60 No causal relation between HGV and hepatitis has been established.

61 tment clinical features were similar between HGV RNA-positive and -negative patients.

62 ient and graft survival were similar between HGV-positive and HGV-negative patients.

63 Both HGV-positive and -negative groups had similar survival,

64 ted using branched DNA (bDNA) assay for both HGV and HCV in the liver explants and pretransplant seru

65 ially reduced or eliminated contamination by HGV RNA sequences.

66 donors, and 230 donors of blood received by HGV-infected patients were tested for HGV RNA by qualita

67 te counts, and 12-year AIDS-free survival by HGV positivity (viremia [RNA] or anti-E2 antibodies).

68 sociated with hepatitis in humans, and GBV-C/HGV coinfection is common in patients chronically infect

69 GBV-C/HGV infection also had no significant impact on the post

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

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

72 GBV-C/HGV infection was not related to the number of blood pro

73 namese were tested for the presence of GBV-C/HGV RNA by the reverse transcription polymerase chain re

74 n-alpha and ribavirin therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and quantitat

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

76 therapy on serum GBV-C/HGV RNA levels, GBV-C/HGV RNA was detected and quantitated in serum samples fr

77 t usually transient reduction in serum GBV-C/HGV RNA, and ribavirin had, at most, a modest antiviral

78 y: 10 patients were positive for serum GBV-C/HGV RNA.

79 lence of GB virus-C/hepatitis G virus (GBV-C/HGV) infection in liver transplant recipients transplant

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

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

82 stologic features of the patients with GBV-C/HGV-HCV coinfection compared with those with HCV infecti

83 To characterize HGV particle types, we evaluated plasma from chronically

84 Chronically HGV-infected individuals contained antibody to the HGV c

85 Plasma samples from chronically HGV-infected individuals and controls were assessed by a

86 regions of the United States had circulating HGV RNA.

87 We investigated the presence of circulating HGV in 36 patients with well-documented non-A-E fulminan

88 d immunoassay to determine if they contained HGV antibody specific for a conserved region in the codi

89 First, could HGV coinfection play any role in the response of HCV to

90 Patients with past or current HGV infection have higher CD4+ lymphocyte counts and bet

91 assay for HGV-RNA, we were unable to detect HGV-RNA within the livers of patients with cryptogenic c

92 t one third of recipients who had detectable HGV RNA in the first month after OLT.

93 ed blood donors (1.4 percent) had detectable HGV RNA.

94 was found to be most efficient in detecting HGV and was subsequently used to test 162 HCV-positive a

95 tion and its association with liver disease, HGV RNA was assessed in the most recent serum sample for

96 Among non-renumerated UK blood donors HGV infection (detected by PCR) was more common than HCV

97 d and shared common parenteral risk factors; HGV did not appear to cause hepatitis or to worsen the c

98 nd a commercially available RT-PCR assay for HGV or GBV-C gave concordant results for 96% of the pati

99 cription-polymerase chain reaction assay for HGV-RNA, we were unable to detect HGV-RNA within the liv

100 s drug abuse was the leading risk factor for HGV transmission, followed by blood transfusion, snortin

101 ards models, risk for AIDS was 40% lower for HGV-positive patients independent of age, HIV and HCV vi

102 opism, but this pattern was not observed for HGV.

103 ted concentrates, 13 (14%) were positive for HGV compared with 79 (83%) who were positive for HCV.

104 these 25 positive patients were positive for HGV or GBV-C by the commercial RT-PCR assay.

105 t significantly different) were positive for HGV RNA in serum.

106 ut 75 percent were persistently positive for HGV RNA, as were 87 percent of those with both hepatitis

107 one of 6 patients with EMC were positive for HGV RNA, for an overall prevalence of 3.0% in mixed cryo

108 ts (46%), including 22 who were positive for HGV RNA, had higher CD4+ lymphocyte counts (difference,

109 of the control populations were positive for HGV.

110 erum samples were recoded and reanalyzed for HGV RNA using different primer sets to assess the validi

111 Retesting for HGV RNA with different primers was positive in all but 1

112 iver is not the primary replication site for HGV, at least in a significant proportion of patients.

113 iver is not the primary replication site for HGV, at least in the population of HCV/HGV-coinfected pa

114 of hepatitis G virus (HGV), were tested for HGV or GB virus C (GBV-C) RNA.

115 rom 96 hemodialysis patients were tested for HGV or GBV-C RNA, 25 patients (26%) were positive by the

116 ved by HGV-infected patients were tested for HGV RNA by qualitative and quantitative polymerase-chain

117 d after liver transplantation was tested for HGV RNA by reverse transcriptase (RT)-PCR using primers

118 Serum samples were tested for HGV RNA by the polymerase chain reaction.

119 NA was significantly higher for HCV than for HGV (median 129 and 0.3 respectively, P < .01).

120 iver were consistently higher than those for HGV RNA (median 1.13 x 10(8) and 360,000 Eq/g respective

121 hosis by analyzing archival liver tissue for HGV-RNA in patients undergoing orthotopic liver transpla

122 IDUs) and in prior specimens for those found HGV RNA-positive.

123 The significance of hepatitis G (HGV) infection in liver transplant recipients is not kno

124 etected up to a 9% incidence of hepatitis G (HGV)-RNA in patients with acute and chronic liver diseas

125 There was no difference between the groups (HGV+ vs. HGV-) when baseline alanine aminotransferase (A

126 Initially, 66 (37%) had HGV RNA.

127 ailable in the first postoperative month had HGV infection.

128 Similar to HCV, HGV particles included an extremely-low-density virion p

129 ed with hepatitis C, patients with mixed HCV-HGV infections did not demonstrate a more severe course

130 e for HGV, at least in the population of HCV/HGV-coinfected patients.

131 ples from 30 transplant recipients: Group I, HGV/HCV coinfection (n = 10); group II, HCV infection al

132 II, HCV infection alone, (n = 8); group III, HGV alone (n = 12).

133 m this surveillance study does not implicate HGV as an etiologic agent of non-A-E hepatitis.

134 e two groups (38% in HGV-positive and 22% in HGV-negative patients).

135 ficantly different in the two groups (38% in HGV-positive and 22% in HGV-negative patients).

136 Changes in HGV-RNA levels were evaluated before, during, and after

137 There was no significant difference in HGV positivity between patients treated before the intro

138 There was no difference in HGV positivity rates between those with normal AST level

139 al therapy appeared to induce a reduction in HGV-RNA load in five of nine patients coinfected with HC

140 Although hepatitis G virus infection (HGV) is usually asymptomatic, it has been associated wit

141 in 9 donors (1.5%); 8 of 9 subsequently lost HGV RNA but anti-E2 persisted.

142 Mean HGV RNA levels were 9.8 (+/-4.2) (viral molecular equiva

143 ipients persistently infected with HGV, mean HGV RNA titers increase after OLT.

144 c recipients who continue to have measurable HGV RNA, three have unexplained hepatitis histologically

145 following liver transplantation, we measured HGV RNA by polymerase chain reaction in pre and posttran

146 detectable in the first postoperative month, HGV RNA fell to undetectable levels at the most recent f

147 Most HGV infections were not associated with hepatitis.

148 centrated in cryoglobulins, and HCV, but not HGV, correlated with cryoglobulinemia in a longitudinal

149 In coinfected sera, HCV, but not HGV, was concentrated in cryoglobulins, and HCV, but not

150 ined, although prevalences as high as 43% of HGV infections in type II cryoglobulinemia have also bee

151 significantly higher rate of acquisition of HGV infection following transplantation (53%, P < .001)

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

153 t- and long-term rates of sequence change of HGV/GBV-C violates the assumptions of the "molecular clo

154 terogeneity consistent with the existence of HGV genetic groups or types.

155 Clinical and biochemical features of HGV-positive and HCV-positive patients and patients with

156 The finding of HGV RNA in serum from these patients is likely related t

157 inoculated with approximately 10(4.7) GE of HGV had late appearance (week 7 pi) of viremia.

158 inoculated with approximately 10(6.7) GE of HGV had viremia at week 1 pi.

159 proximately 10(8) genome equivalents (GE) of HGV.

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

161 rs, clinical significance, and the impact of HGV on coexistent hepatitis C virus (HCV).

162 ed the prevalence of persistent infection of HGV and HCV in patients exposed to non-virus-inactivated

163 ay explain the reported lack of influence of HGV coinfection on the course of chronic hepatitis C.

164 liver disease and examined the influence of HGV coinfection on the outcome of liver transplantation.

165 m = 500,000 vs. 200,000 Eq/mL) and levels of HGV RNA in liver and serum were similar in patients with

166 NS4A of HGV was demonstrated to be a cofactor for NS3-mediated p

167 re is no association between the presence of HGV coinfection and the severity of liver disease post-t

168 We searched for the presence of HGV RNA and HCV RNA sequences in liver and serum samples

169 was no relationship between the presence of HGV RNA and the presence of posttransplantation liver di

170 The presence of HGV RNA in prediagnostic serum was not associated with t

171 The prevalence of HGV co-infection was 21% before transplantation and 22%

172 The prevalence of HGV in a group of multitransfused patients with hematolo

173 suggest the following: 1) The prevalence of HGV infection in patients undergoing OLT for cryptogenic

174 The preoperative prevalence of HGV infection in recipients transplanted for cryptogenic

175 ents were HGV positive and the prevalence of HGV infection was similar for different HCV genotypes.

176 The prevalence of HGV RNA was determined in samples collected before and a

177 Consequently, the biophysical properties of HGV may be very different from those of HCV.

178 The prevalence rate of HGV RNA in transplanted controls was 64% (P < .01) with

179 The overall prevalence rate of HGV RNA in transplanted patients with chronic hepatitis

180 The median liver/serum ratio of HGV RNA was less than unity, a finding consistent with s

181 at least part of the putative core region of HGV is expressed in vivo.

182 Inconsistent results of HGV and the risk of hepatocellular carcinoma (HCC) have

183 We sought to clarify the role of HGV as a causative agent in cryptogenic cirrhosis by ana

184 , China, was conducted to assess the role of HGV infection in HCC development.

185 ver disease of unknown cause and the role of HGV infection in posttransplantation hepatitis, we studi

186 clude that the liver is not the main site of HGV replication.

187 eled the levels of HCV RNA, but not those of HGV RNA.

188 , the pre- and postoperative viral titers of HGV, and the allograft histology in patients infected wi

189 rom all donors could be tested, at least one HGV-positive donor was identified.

190 HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected)

191 ology occurs in 60% (3 of 5) of persistently HGV-infected cryptogenic recipients.

192 f pretransplantation and posttransplantation HGV infection was 24% and 28%, respectively.

193 sitively correlated with posttransplantation HGV infection (P < 0.001).

194 18 months after disease onset, have remained HGV RNA-positive but have become HCV RNA-negative.

195 Serum HGV RNA and hepatitis B surface antigen (HBsAg) were ass

196 Serum HGV RNA was determined by reverse transcriptase-polymera

197 Serum HGV titer increased steadily until it plateaued at 10(6)

198 ents with HCV infection had detectable serum HGV-RNA.

199 trol subjects (3.2%) were positive for serum HGV RNA.

200 In two patients, the fall in serum HGV-RNA correlated with biochemical response, independen

201 coinfected population have changes in serum HGV-RNA induced by interferon.

202 cantly associated with the presence of serum HGV RNA (P <.02).

203 Negative-strand HGV RNA was detected in three of four bone marrow sample

204 In summary, HGV and HCV infections were frequently associated and sh

205 This study does not support HGV as a primary hepatotropic virus.

206 It is concluded that HGV infection plays no role in HCC development in this h

207 These data indicate that HGV has a nucleocapsid and that at least part of the put

208 ing infected with HGV alone, suggesting that HGV is not the main etiologic agent of non-A-E hepatitis

209 had fewer years of drug use, suggesting that HGV RNA had previously been cleared.

210 fference between the particle types was that HGV was consistently more stable in cesium chloride than

211 The HGV nucleotide and protein sequences obtained in this st

212 The HGV sequences obtained from one patient showed no change

213 on 10-fold serial dilutions of RNA from the HGV reference strain, the last positive dilution was 10(

214 no significant variations were found in the HGV nucleotide and derived amino acid sequences over tim

215 s based on the 5'-untranslated region of the HGV genome.

216 T)-PCR using primers to the 5' region of the HGV genome.

217 ion using primers from the NS5 region of the HGV genome.

218 ions from 6 known full-size sequences of the HGV genomes demonstrated notable discrete heterogeneity

219 nt core protein at the amino terminus of the HGV polyprotein.

220 nt primer sets to assess the validity of the HGV RNA assay.

221 livers were negative for the presence of the HGV RNA minus strand and only six were positive for the

222 tients were negative for the presence of the HGV RNA minus strand in the liver when tested with a str

223 fected individuals contained antibody to the HGV core protein peptide, whereas no binding to a hepati

224 udy hepatitis G virus (HGV), antibody to the HGV envelope protein (anti-E2), risk factors, clinical s

225 Competitive inhibition of binding to the HGV peptide confirmed the specificity of the assay.

226 After therapy, HGV RNA levels returned to baseline in most subjects.

227 Thus, HGV infection is common among HIV-infected homosexual ma

228 Thus, HGV is frequently found in transplantation patients co-i

229 rom archival paraffin-embedded liver tissue; HGV sequences were amplified by nested reverse transcrip

230 This lends further evidence to HGV infection not being a cause of cryptogenic cirrhosis

231 rences utilized during in vitro translation, HGV appears to have a truncated or absent core protein a

232 Pre-transplantation HGV infection was positively correlated with posttranspl

233 Two HGV proteases similar to nonstructural proteins NS2 and

234 In serial specimens obtained from the two HGV-infected patients, no significant variations were fo

235 hat all but two positive patients had unique HGV or GBV-C sequences.

236 Hepatitis G virus (HGV or GB-C virus) is a newly described virus that is cl

237 It is unclear whether hepatitis G virus (HGV) can lead to chronic liver disease and cirrhosis.

238 o tested positive for the hepatitis G virus (HGV) did not have a significantly increased risk of CLD,

239 om a 2.6-kb region of the hepatitis G virus (HGV) genome at nucleotide positions 5829 to 8421 were de

240 examine the prevalence of hepatitis G virus (HGV) in end-stage liver disease of unknown cause and the

241 e pathogenic role for the hepatitis G virus (HGV) in patients with cryptogenic fulminant hepatitis (n

242 The role of hepatitis G virus (HGV) in transfusion-associated infection and its relatio

243 ntrast to HCV, a role for hepatitis G virus (HGV) in type II cryoglobulinemia has not been defined, a

244 assess the persistence of hepatitis G virus (HGV) infection and its association with liver disease, H

245 athogenic implications of hepatitis G virus (HGV) infection are still unclear.

246 The role of hepatitis G virus (HGV) infection in acute non-A-E hepatitis was investigat

247 ermined the prevalence of hepatitis G virus (HGV) infection in end-stage hepatitis C virus (HCV)-rela

248 he health consequences of hepatitis G virus (HGV) infection in humans remain to be determined.

249 lence and consequences of hepatitis G virus (HGV) infection were determined in 180 patients with huma

250 Hepatitis G virus (HGV) is a newly described RNA virus that is parenterally

251 Hepatitis G virus (HGV) is a newly described virus that has been implicated

252 Hepatitis G virus (HGV) is prevalent in patients with chronic liver disease

253 Hepatitis G virus (HGV) is transmissible by blood transfusion, but its role

254 The recently discovered hepatitis G virus (HGV) or GB virus C (GBV-C) is widely distributed in huma

255 f the recently discovered hepatitis G virus (HGV) remain unknown.

256 n of the newly discovered hepatitis G virus (HGV) to the cause and clinical course of acute and chron

257 Hepatitis G virus (HGV) was transmitted to 2 chimpanzees by inoculation wit

258 Hepatitis G virus (HGV), a positive sense RNA virus, is distantly related t

259 Infection with hepatitis G virus (HGV), also known as GB virus C, is prevalent but is not

260 alyses were used to study hepatitis G virus (HGV), antibody to the HGV envelope protein (anti-E2), ri

261 gest that TTV, similar to hepatitis G virus (HGV), may be an example of a human virus with no clear d

262 ecently identified virus, hepatitis G virus (HGV), shows considerable homology to hepatitis C virus (

263 An RNA virus, designated hepatitis G virus (HGV), was identified from the plasma of a patient with c

264 rom a reference strain of hepatitis G virus (HGV), were tested for HGV or GB virus C (GBV-C) RNA.

265 s no difference between the groups (HGV+ vs. HGV-) when baseline alanine aminotransferase (ALT) value

266 onors with confirmed HCV infection, 12% were HGV RNA-positive and 44% were anti-E2-positive (total ex

267 nts, 16 of whom were HGV-positive and 9 were HGV-negative.

268 Forty-one (25.3%) patients were HGV positive and the prevalence of HGV infection was sim

269 a bone marrow transplantation procedure were HGV positive compared with 9 of 27 (33%) treated with co

270 ity-acquired non-A, non-B hepatitis who were HGV RNA positive.

271 on hepatitis in 25 patients, 16 of whom were HGV-positive and 9 were HGV-negative.

272 We sought to determine whether HGV was hepatotropic and to determine whether coinfectio

273 n 4 of the 11 cryptogenic recipients in whom HGV RNA was detectable in the first postoperative month,

274 ic and to determine whether coinfection with HGV and hepatitis C virus (HCV) influenced the level of

275 here is a low prevalence of coinfection with HGV in patients with mixed cryoglobulinemia and HCV infe

276 Coinfection with HGV occurs in 10% to 20% of HCV-infected subjects.

277 Compared with HGV-negative patients, the 60 HGV-positive patients (46%

278 howed high frequencies of contamination with HGV (16 of 17 factor VIII batches positive; six of six f

279 gamma-glutamyl transpeptidase in donors with HGV infection alone or those coinfected with HCV.

280 fusion recipients; only 3 had hepatitis with HGV as the sole viral marker.

281 patient was confirmed as being infected with HGV alone, suggesting that HGV is not the main etiologic

282 llograft histology in patients infected with HGV who underwent OLT for cryptogenic cirrhosis.

283 2) In recipients persistently infected with HGV, mean HGV RNA titers increase after OLT.

284 tested (10 percent) were also infected with HGV.

285 Infection with HGV is common in end-stage HCV-infected patients present

286 Infection with HGV may affect the risk for AIDS in HIV-infected persons

287 Persistent infection with HGV was common, but it did not lead to chronic disease a

288 The three patients infected only with HGV had mild hepatitis (mean peak alanine aminotransfera

289 acute illness were similar for patients with HGV alone and those with hepatitis A, B, or C with or wi

290 did not develop in any of the patients with HGV alone, but 75 percent were persistently positive for

291 iver and serum were similar in patients with HGV infection alone compared to those with HGV/HCV coinf

292 ificantly lower in the control patients with HGV infection alone following transplantation than in pa

293 higher in liver biopsies from patients with HGV infection than in those without HGV infection (2 [ra

294 Three patients with HGV-HCV coinfection, tested within 18 months after disea

295 s with HCV infection alone versus those with HGV/HCV coinfection (median; liver = 1.15 x 10(7) vs. 1.

296 h HGV infection alone compared to those with HGV/HCV coinfection (median; liver = 1.2 x 10(6) vs. 4.0

297 patients infected with HCV with and without HGV infection.

298 t survival between patients with and without HGV infection.

299 se with hepatitis A, B, or C with or without HGV infection.

300 nts with HGV infection than in those without HGV infection (2 [range, 0-14] and 1 [range, 0-3]; P = .