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PubMed2005

What you need to know about GB virus C.

GB virus C (GBV-C) is a nonpathogenic member of the Flaviviridae family most closely related to hepatitis C virus (HCV). Infection is common in healthy and immunocompromised people and may persist for years. GBV-C infection is associated with improved survival, improved AIDS-free survival, higher CD4(+) T-cell counts, and lower HIV viral loads in HIV-infected people compared with people infected with HIV but not GBV-C. The mechanism of this effect is not yet clear, but GBV-C has been shown to inhibit HIV replication in vitro through increased synthesis and secretion of anti-HIV b-chemokines MIP-1a, MIP-1b, RANTES, SDF-1, and SDF-2 and downregulation of CCR5 receptor expression. GBV-C also inhibits apoptosis of its host cell, similar to HCV. GBV-C E2 protein in serum has also been associated with prolonged survival in HIV infection; recent evidence indicates that GBV-C E2 protein may neutralize HIV infection in vitro.

AIDS-Related Opportunistic Infections↗
PubMed2002

Effects of co-infection with hepatitis C virus and GB virus C on CD4 cell count and HIV-RNA level among HIV-infected patients treated with highly active antiretroviral therapy.

The effects of co-infection with hepatitis C virus (HCV) and GB virus C (GBV-C) on CD4 cell counts and plasma HIV-RNA levels has been investigated in HIV-infected patients treated with highly active antiretroviral therapy (HAART). Patients co-infected with HCV and GBV-C experienced a CD4 cell increase during 4 years of HAART, whereas the increase stopped after 2 years in the other groups.

Adult↗
PubMed2003

GB virus C genotype determination in GB virus-C/HIV co-infected individuals.

Several recent studies have indicated that patients infected with human immunodeficiency virus (HIV) exhibit a beneficial effect of co-infection with GB virus C (GBV-C). The benefit is demonstrated by slower progression to acquired immunodeficiency syndrome (AIDS) and prolonged survival time after the development of AIDS. In some but not all studies, a significant association between GBV-C/HIV co-infection and increased CD4(+) cell counts has been reported. To understand further the possible role that GBV-C might play in the reduced morbidity and mortality among HIV-infected patients, we sought to examine the presence of different GBV-C genotypes in a cohort of co-infected patients. PCR products derived from the 5'-untranslated region (5'-UTR) and the second envelope gene (E2) were sequenced directly and genotyped by phylogenetic analysis. While 5'-UTR analysis delineated the major type, analysis of the complete E2 gene was required for identification of group 2 subtypes, designated 2a and 2b. Among 35 patients tested, GBV-C genotype was determined for 33: two patients were infected with genotype 1, 12 with type 2a, and 19 with type 2b. Clinical data were available for 25 genotyped patients: one infected with genotype 1, nine with genotype 2a, and 15 with type 2b. CD4 cell counts tended to be lower in patients infected with genotype 2a compared with those with genotype 2b (310 +/- 136 vs 430 +/- 199, P = 0.054). Additional studies with larger cohorts from separate geographical regions are needed to determine whether a particular GBV-C genotype is associated with reduced morbidity or mortality among HIV co-infected patients.

5' Untranslated Regions↗
PubMed1998

Antibodies against the GB virus C envelope 2 protein before liver transplantation protect against GB virus C de novo infection.

GB virus C (GBV-C) is a newly discovered RNA virus related to the Flaviviridae family. Although GBV-C is not yet associated with any cause of liver disease, a humoral immune response against the GBV-C envelope 2 (E2) protein has been observed. Therefore, we studied the prevalence and clinical relevance of GBV-C RNA and anti-E2 antibodies in patients undergoing orthotopic liver transplantation (OLT). In addition, we tested whether the prevalence of anti-E2 antibodies may protect against GBV-C infection. Of the 182 liver recipients included in this study, 117 of these were evaluated for GBV-C recurrence or de novo infection. GBV-C RNA was detected in sera or plasma using single-tube, reverse-transcriptase polymerase chain reaction, and anti-E2 antibody was detected by enzyme immunoassay (EIA). Cumulative patient and graft survival was tested by using Kaplan-Meier analysis. The independence of prognostic values was assessed by using Cox regression analysis. Before OLT, GBV-C RNA and anti-E2 were detected in 4.0% to 28.6% and 10.0% to 68.8%, respectively, of patients suffering from different forms of chronic liver diseases. GBV-C reinfection after OLT was determined in 85.7%. Of the patients without evidence of exposure to GBV-C before OLT, 30 of 65 (46.2%) became GBV-C RNA positive after OLT. None of the 38 patients who were anti-E2 antibody positive before OLT became GBV-C RNA positive after OLT. Neither patient nor graft survival was significantly affected by the presence of either GBV-C RNA or anti-E2 antibody before OLT. Our data indicate that 1) GBV-C RNA positive patients have a high risk of reinfection after OLT, and 2) the presence of anti-E2 antibodies before OLT is associated with an absence of GBV-C infection after OLT, which may indicate a protective role of anti-E2 antibodies.

Adult↗
PubMed1998

Influence of GB virus C viraemia on the clinical, virological and histological features of early hepatitis C-related hepatic disease.

BACKGROUND/AIMS: GB virus C is a newly described RNA virus. The aims of this study were to determine the prevalence of GB virus C infection in patients with chronic type C hepatitis and to examine the clinical, virological and histological features in hepatitis C and GB virus C co-infected patients. METHODS/RESULTS: One hundred and sixty patients with hepatitis C infection were studied. GBV-C RNA was detected in 33/160 (20.6%) patients; co-infected patients with hepatitis C and GB virus C infection were significantly younger (p=0.04). No difference was found between the two groups according to gender and biochemical parameters. Seventy-two of the 160 patients, for whom a liver tissue specimen taken simultaneously with the serum was available and who had compensated liver disease, were studied separately. The source of infection, duration of infection, HCV genotype and HCV RNA concentrations did not differ between 15/72 patients with dual infection and 57/72 with hepatitis C infection alone. Patients with co-infection had significantly higher degrees of portal and periportal inflammation (p=0.0006 and 0.01, respectively). No difference was observed in parenchymal activity score or extent of fibrosis. CONCLUSIONS: These results indicate a relatively high prevalence of GB virus C infection in younger patients with chronic hepatitis C, suggesting a common route of transmission. Although GB virus C co-infection does not alter the biochemical and virological profile of patients with HCV hepatitis, there is an association between GB virus C and hepatitis C viraemia and portal and periportal inflammation.

Adult↗
PubMed1999

Dynamics of GB virus C viremia early after orthotopic liver transplantation indicates extrahepatic tissues as the predominant site of GB virus C replication.

The principal site of GB virus C (GBV-C) replication is unknown. To determine whether hepatic GBV-C replication is important for the maintenance of a measurable viremia level in GBV-C infection, the influence of hepatectomy followed by liver transplantation on GBV-C viremia was investigated. GBV-C RNA levels were determined by a quantitative TaqMan polymerase chain reaction (PCR) in 12 patients with pretransplantation GBV-C infection before and daily after orthotopic liver transplantation (OLT) for 25 to 28 days. Compared with the pretransplantation values (mean, 12.4 +/- 3.9 x 10(7) copies/mL), mean GBV-C RNA levels declined significantly by 1 log by day 1 after OLT (mean, 3.5 +/- 1.6 x 10(7) copies/mL), but subsequently remained relatively stable on this high level for the entire observation period, indicating ongoing high-level virus replication (mean GBV-C RNA levels on days 7 and 28 were: 1.7 +/- 0. 5 x 10(7) and 2.8 +/- 0.7 x 10(7) copies/mL; P = ns). Thus, at the end of the follow-up, mean GBV-C RNA levels were not significantly different from that of the 1st and 7th postoperative day and remained significantly lower compared with the pretransplantation values. However, in 2 of the 12 patients, different kinetics were observed. Both already had low-level viremia pre-OLT (0.02 and 0.002 x 10(7) copies/mL) and became persistently GBV-C RNA-negative 2 days after OLT. In 5 patients, liver tissues were collected 6 to 9 days after OLT and investigated for GBV-C RNA. All but 1 were GBV-C RNA-negative in the liver, although 2 of them had rather high serum GBV-C RNA levels at this time. The kinetics of GBV-C viremia observed in our study were neither influenced by the immunosuppressive therapy nor by the number of blood and blood product transfusions given after OLT. In addition, they were quite different from those observed in patients with chronic hepatitis C in whom early reinfection of the graft could be demonstrated by a steady increase in HCV RNA levels starting 3 days after OLT and exceeding preoperative levels by day 8. From our data, one can conclude that the liver is certainly not the major site of GBV-C replication in most patients. However, one cannot exclude that host or viral factors exist that predispose GBV-C replication predominantly in the liver.

Adult↗
PubMed1996

Sequence heterogeneity within the 5'-terminal region of the hepatitis GB virus C genome and evidence for genotypes.

BACKGROUND: GB virus C is a positive-strand RNA virus that is associated with hepatitis in humans. GB virus C bears some resemblance to hepatitis C virus in its genomic sequence and organization. However, unlike hepatitis C virus, an open reading frame possessing a complete core protein was not identified in the original isolate. METHODS: To verify the sequence at the 5'-end of the GB virus C genome, we amplified approximately 600 nucleotides from this region from 35 globally distributed individuals. The nucleotide sequences were translated in all possible reading frames and then examined for conserved motifs indicative of nucleocapsid or core-like peptides. RESULTS: Forty-two unique GB virus C sequences were obtained from the 35 individuals. The deduced amino acid sequences upstream of the putative E1 gene from each isolate varied in length and composition, such that a conserved core-like sequence was not apparent. No core-like sequences were evident in the other reading frames. There was, however, a single methionine codon held in common among all isolates, although it was located very near the presumed amino-terminus of the putative E1 protein. Further analysis of the sequences for their evolutionary relatedness demonstrated the existence of five GB virus C subtypes that demonstrated a significant correlation with geographic distribution. CONCLUSIONS: GB virus C differs from hepatitis C virus and GB virus B in that it does not encode a nucleocapsid or core protein. The existence of GB virus C subtypes emphasizes the importance of investigating the correlation between infecting subtype and the severity of liver disease and/or responsiveness to treatment of GB virus C-associated hepatitis.

Base Sequence↗
PubMed2006

Effect of primer selection on estimates of GB virus C (GBV-C) prevalence and response to antiretroviral therapy for optimal testing for GBV-C viremia.

GB virus C (GBV-C; also called hepatitis G virus) is a common cause of infection associated with prolonged survival among HIV-infected individuals. The prevalences of GBV-C viremia vary widely in different studies, and there has been poor agreement among different laboratories performing GBV-C RNA detection in quality control studies. To determine the optimal method of measuring GBV-C RNA in clinical samples, samples obtained from 939 HIV-infected subjects were studied using reverse transcription (RT)-PCR methods amplifying four separate regions of the GBV-C genome. Primers amplifying the E2 coding region were 100% specific; however, their sensitivity was only 76.6%. In contrast, primers amplifying three additional conserved regions of the GBV-C genome (the 5' nontranslated region and the nonstructural protein-coding regions 3 and 5A) were more sensitive but produced higher rates of false-positive results. Using low-specificity primer sets influenced the significance of association between GBV-C viremia and response to antiretroviral therapy. Using a quantitative GBV-C RNA method, the GBV-C RNA concentration did not correlate with baseline or set point HIV RNA levels; however, a correlation between negative, low, and high GBV-C RNA levels and increasing reduction in HIV RNA following antiretroviral therapy was observed. Subjects with both GBV-C E2 antibody and viremia had significantly lower GBV-C RNA levels than did viremic subjects without E2 antibody. These studies demonstrate that accurate detection of GBV-C RNA by nested RT-PCR requires the use of primers representing multiple genome regions. Analyses based on testing with single primers do not lead to reliable conclusions about the association between GBV-C infection and clinical outcomes.

Anti-HIV Agents↗
PubMed1999

Little contribution of GB virus C to the development of primary hepatocellular carcinoma in Japan.

RNA of GB virus C was searched for in sera from 109 patients with primary hepatocellular carcinoma. It was detected in 11 patients (10%), and was more frequent than in 3 of 342 blood donors (0.9%) (P < 0.001). The 11 patients included 4 of 29 patients (14%) with hepatitis B surface antigen and 7 of 74 patients (9%) with antibody to hepatitis C virus. RNA of GB virus C was not detected in any of 4 patients without hepatitis B surface antigen or antibody to hepatitis C virus. These results suggest that GB virus C may contribute little to the development of primary hepatocellular carcinoma in Japan.

Carcinoma, Hepatocellular↗
PubMed1997

Evaluation of four PCR systems amplifying different genomic regions for molecular diagnosis of GB virus C infections.

Diagnosis of GB virus C (GBV-C) infection is based on RT-PCR methodology that detects genomic viral RNA. Four sets of primers located in different genomic regions were compared. These primers were used to amplify a reference panel of sera used by the French blood banks, including five positive sera, five negative sera and 10-fold serial dilutions of one positive serum. Three sets of primers located in the 5'UTR, NS3 and NS5a genomic regions gave comparable results with undiluted sera. When diluted sera were tested, the most sensitive protocol was that using a set of primers and a probe selected within the 5'UTR, together with a colorimetric detection based on DNA enzyme immunoassay.

Evaluation Studies as Topic↗
PubMed1999

GB virus C infection: clinical significance.

GB virus C (GBV-C) RNA positivity rates were examined in serum specimens from 231 patients with liver disease (23 patients with hepatitis B, 175 patients with hepatitis C, five patients with hepatitis B virus plus hepatitis C virus coinfection, and 28 patients with non-A, non-B, non-C hepatitis) to clarify the clinical significance of this virus. GBV-C RNA was detected in none of 12 patients with fulminant hepatitis, one of two patients with acute hepatitis positive for hepatitis B surface antigen and one of four patients with acute non-A, non-B, non-C hepatitis. Pathogenetic involvement of GBV-C was suspected in some patients in the latter group. Among patients with the non-B, non-C type of chronic disease, one of seven with cirrhosis (14%) and none with chronic hepatitis or hepatocellular carcinoma were GBV-C-positive. In chronic hepatitis C patients who had received interferon treatment, no difference was found in clinical findings, alanine aminotransferase (ALT) concentrations, histology or response to interferon between 11 patients who were GBV-C RNA-positive and 101 patients who were GBV-C RNA-negative. Moreover, changes in ALT after interferon therapy showed no relation to positivity for GBV-C RNA. On the basis of these findings, GBV-C appears to be an unlikely cause of initiation or progression of chronic hepatic diseases.

Adult↗
PubMed2005

Male to male sex is associated with a high prevalence of exposure to GB virus C.

Co-infection with GB virus C (GBV-C) and human immunodeficiency virus (HIV) appears to reduce mortality for HIV/AIDS. Epidemiological and demographic factors for GBV-C were examined prospectively in 167 subjects at risk for co-infection. We attempted to establish a hierarchical exposure risk for GBV-C. Overall exposure to GBV-C was 45.5%. In univariate analysis, GBV-C was associated with male to male sex (P<0.0001), HIV infection (P=0.0005) and hepatitis B infection (P=0.006). Injecting drug use approached statistical significance (P=0.08) while being a female sex worker was not associated with GBV-C exposure/infection (P=0.85). Exposure to GBV-C in 192 healthy blood donors was found to be 9.4%. In conclusion, the data suggest that male to male sex is a more effective mode of transmission of GBV-C and that GBV-C is associated with HIV co-infection. As male to male sex is also a risk factor for HIV transmission our data suggest that many may benefit from the potential protective effect GBV-C exerts on HIV-infected persons.

Adult↗
PubMed2005

GB virus C: insights into co-infection.

GB virus C (GBV-C) is a single stranded positive sense RNA virus, which is a member of the Flaviviridae. It has a close sequence homology and genomic organisation to hepatitis C virus (HCV). However, unlike HCV it is not hepatotrophic. GBV-C replicates within cells of the haemopoietic lineage, in particular lymphocytes. No disease has been associated with GBV-C infection but co-infection with human immunodeficiency virus (HIV) leads to improved morbidity and mortality for the HIV infected individual and slows progression to acquired immunodeficiency syndrome. This potential benefit of GBV-C has been demonstrated in the pre and post highly active anti-retroviral treatment (HAART) eras. GBV-C has been found to decrease HIV replication in in vitro models. The mechanism of the beneficial effect of GBV-C appears to be mediated by alterations in the cellular immune response, the details of which remain unclear. Despite this, there continues to be controversy regarding the influence of GBV-C on HIV as several reports have questioned the beneficial effect. GBV-C does not appear to influence liver related disease in subjects co-infected with HCV or hepatitis B virus (HBV). Combination of HIV and HCV leads to accelerated liver disease. The influence of GBV-C in this situation is yet to be determined. Elucidation of the putative protective effect of GBV-C in HIV co-infection could potentially identify novel targets for anti-HIV therapeutics and lead to the development of disease modifying vaccines.

Flaviviridae Infections↗
PubMed1999

Possible association between serum GB virus C RNA level and disease activity in fulminant hepatitis type G.

BACKGROUND/AIMS: Whether GB virus C causes serious liver diseases remains controversial. The aim of the present study was to determine whether there is an etiological relationship between GB virus C and fulminant hepatitis. METHODS: The level of GB virus C RNA in the sera of three patients with fulminant hepatitis was quantitatively determined using the newly developed real-time detection polymerase chain reaction method, which is based on Taq Man chemistry. The NS 3 region of the viral genome isolated from the sera was sequenced at several time points to confirm whether the same virus was responsible for fulminant hepatitis during the patients' clinical courses. RESULTS: The sensitivity of the PCR was comparable to that of nested PCR and a linear relationship between RNA copy number and threshold cycle was observed for 10(1) and 10(6) RNA copies/ml (r = 0.99). The serum level of GB virus C RNA closely paralleled that of ALT in all patients. Sequence analysis of the NS3 region isolated from the patients' sera revealed that the same GB virus C strain infected the patients during their entire clinical courses, despite plasma exchange therapy. CONCLUSIONS: These observations suggest that GB virus C may be etiologically associated with fulminant hepatic failure, and is not merely an inactive bystander introduced by therapeutic plasma exchange.

Adult↗
PubMed2004

GB virus C infection and quality of life in HIV-positive patients.

It was recently shown that GBV-C infection is associated with prolonged survival of HIV-infected individuals. The GB virus C is the closest known relative of hepatitis C virus in man. The latter has been associated with significant impairment in quality of life, independent from the associated liver disease. We were thus interested in the impact of GB virus C infection on quality of life in HIV-infected individuals. We retrospectively analyzed a cohort of HIV-positive patients who previously answered the 'HIV-SELT' and the 'EQ-5D' questionnaires assessing quality of life and for whom data on GB virus C RNA status were available. In this study we identified no adverse effect of GB virus C on quality of life, but, in contrast, GB virus C viraemic patients showed better quality of life in all parameters for the scores in comparison to GB virus C-negative HIV-infected patients. HIV-positive patients with a GB virus C infection showed superior quality of life. These data further support the favourable course of HIV disease in GB virus C-positive patients.

Adult↗
PubMedDate not supplied

GB virus C infection by blood transfusion during and following liver surgery.

BACKGROUND/AIMS: GB virus C has been associated with some cases of fulminant hepatitis and post-transfusion hepatitis. We examined transfusion-related infection with this virus. METHODOLOGY: Of 150 patients undergoing liver resection, 108 received a homologous blood transfusion. Serum samples before and after surgery were examined for GB virus C RNA by a nested polymerase chain reaction with reverse transcription. We also studied the post-operative course of patients infected with GB virus C by blood transfusion. RESULTS: Viral RNA was detected in sera taken after transfusion in 4 (4%) patients receiving homologous transfusions. Viral RNA was not detected after surgery in the 42 patients given autologous transfusions or not receiving homologous blood. Post-operative courses in the 4 infected patients were uneventful. CONCLUSIONS: As 4% of homologous transfusions resulted in GB virus C infection in our small surgical study, autologous transfusion is recommended when circumstances permit.

Blood Transfusion↗
PubMed1999

Amino acid substitutions in NS5A region of GB virus C and response to interferon therapy.

GB virus C (GBV-C) is related to hepatitis C virus (HCV) and has a similar genomic structure. Some predictors for the efficacy of interferon (IFN) therapy on HCV have been reported: genotype, viral load, IFN dose, and the amino acid substitutions in the NS5A region, designated as the interferon sensitivity determining region (ISDR). To evaluate the correlation between the amino acid substitutions in the GBV-C NS5A region and the response to IFN therapy, single-strand conformation polymorphism (SSCP) analysis was performed in the 12 concomitantly GBV-C-and HCV-infected patients who received IFN therapy at three time points: before, end-point, and after the IFN therapy. The region in the GBV-C NS5A studied includes the amino acids that exhibit some homology to the ISDR and the various substitutions. By SSCP analysis, amplicons were separated into 1-4 bands, which indicated the existence of heterogeneity in each host. However, the deduced amino acid sequences in these bands exhibited no characteristic differences among these strains irrespective of response to IFN therapy. Of the 32 strains separated by SSCP, 7 strains were responders, and 25 were nonresponders. The mean amino acid substitution, compared with the consensus sequence of nonresponders, was 1.00+/-0.93 among responders, and 1.40+/-0.85 among non-responders (P= NS). No correlation between the amino acid sequence in the GBV-C NS5A region and response to IFN therapy was found, indicating that the GBV-C NS5A region dose not act as the ISDR.

Adult↗
PubMed1998

Molecular analysis of GB virus C isolates in Belgian hemodialysis patients.

GB virus C (GBV-C) has been detected in Belgian hemodialysis patients. To study their genomic diversity and phylogenetic relationship, a 592 nucleotide fragment extending from the 5' non-coding region to part of the E1 gene of the GBV-C genome was amplified and sequenced from 12 Belgian hemodialysis patients in two different centers. Together with strains from different geographical origins, these sequences were analyzed phylogenetically using three different methods. A consistent tree topology was obtained with all methods. Three GBV-C genotypes were observed with two subtypes in type 2 and a questionable subtyping in type 1. Except for one isolate falling into type 1 cluster which mainly consists of African strains, all the other Belgian strains clustered within the type 2a branch. Two GBV-C isolates in two patients from the same hemodialysis center clustered together closely, suggesting a nosocomial transmission. In view of their long branch length, it seems unlikely that the other Belgian strains evolved recently from a common ancestor. Our results indicate that the major type circulating among Belgian hemodialysis patients seems to be 2a, which is usual for Europe and North America, but that the African type 1 also exists to a minor extent. Although patient to patient transmission of GBV-C in Belgian hemodialysis centers did occur, it may not account for the majority of infections.

Base Sequence↗