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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
33 Compared with HGV-negative patients, the 60 HGV-positive patients (46%), including 22 who were posit
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
41 serum levels of liver-related enzymes among HGV RNA-positive and -negative participants (P > .20).
43 ervations indicate that a larger study of an HGV population is required to more clearly define the re
47 eron response was similar in both groups and HGV was not associated with outcome following therapy.
49 arly define the relationship between HCV and HGV coinfection and their response to antiviral therapy.
54 HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected) developed light-
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
64 ted using branched DNA (bDNA) assay for both HGV and HCV in the liver explants and pretransplant seru
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
70 To determine the clinical impact of GBV-C/HGV infection in such patients and the effect of interfe
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
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
79 lence of GB virus-C/hepatitis G virus (GBV-C/HGV) infection in liver transplant recipients transplant
82 stologic features of the patients with GBV-C/HGV-HCV coinfection compared with those with HCV infecti
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
91 assay for HGV-RNA, we were unable to detect HGV-RNA within the livers of patients with cryptogenic c
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
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
103 ted concentrates, 13 (14%) were positive for HGV compared with 79 (83%) who were positive for HCV.
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,
110 erum samples were recoded and reanalyzed for HGV RNA using different primer sets to assess the validi
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
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
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
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
129 ed with hepatitis C, patients with mixed HCV-HGV infections did not demonstrate a more severe course
131 ples from 30 transplant recipients: Group I, HGV/HCV coinfection (n = 10); group II, HCV infection al
139 al therapy appeared to induce a reduction in HGV-RNA load in five of nine patients coinfected with HC
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
148 centrated in cryoglobulins, and HCV, but not HGV, correlated with cryoglobulinemia in a longitudinal
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)
153 t- and long-term rates of sequence change of HGV/GBV-C violates the assumptions of the "molecular clo
160 nces (8,500 bases) of different genotypes of HGV/GBV-C showed an excess of invariant synonymous sites
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
167 re is no association between the presence of HGV coinfection and the severity of liver disease post-t
169 was no relationship between the presence of HGV RNA and the presence of posttransplantation liver di
173 suggest the following: 1) The prevalence of HGV infection in patients undergoing OLT for cryptogenic
175 ents were HGV positive and the prevalence of HGV infection was similar for different HCV genotypes.
185 ver disease of unknown cause and the role of HGV infection in posttransplantation hepatitis, we studi
188 , the pre- and postoperative viral titers of HGV, and the allograft histology in patients infected wi
208 ing infected with HGV alone, suggesting that HGV is not the main etiologic agent of non-A-E hepatitis
210 fference between the particle types was that HGV was consistently more stable in cesium chloride than
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
218 ions from 6 known full-size sequences of the HGV genomes demonstrated notable discrete heterogeneity
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
229 rom archival paraffin-embedded liver tissue; HGV sequences were amplified by nested reverse transcrip
231 rences utilized during in vitro translation, HGV appears to have a truncated or absent core protein a
234 In serial specimens obtained from the two HGV-infected patients, no significant variations were fo
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
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
247 ermined the prevalence of hepatitis G virus (HGV) infection in end-stage hepatitis C virus (HCV)-rela
249 lence and consequences of hepatitis G virus (HGV) infection were determined in 180 patients with huma
254 The recently discovered hepatitis G virus (HGV) or GB virus C (GBV-C) is widely distributed in huma
256 n of the newly discovered hepatitis G virus (HGV) to the cause and clinical course of acute and chron
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
269 a bone marrow transplantation procedure were HGV positive compared with 9 of 27 (33%) treated with co
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
278 howed high frequencies of contamination with HGV (16 of 17 factor VIII batches positive; six of six f
281 patient was confirmed as being infected with HGV alone, suggesting that HGV is not the main etiologic
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
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
300 nts with HGV infection than in those without HGV infection (2 [range, 0-14] and 1 [range, 0-3]; P = .
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