Infection with GB virus C (GBV-C) in patients with fulminant hepatitis

Tameda, Yukihiko; Kosaka, Yoshitane; Tagawa, Shoh; Takase, Koujirou; Sawada, Natsumi; Nakao, Haruhisa; Tsuda, Fumio; Tanaka, Takeshi; Okamoto, Hiroaki; Miyakawa, Yuzo; Matsui, Makoto

doi:10.1016/s0168-8278(96)80287-x

Cited by 45 publications

(26 citation statements)

References 16 publications

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“…32 Despite these facts, some authors argue in favor of HGV' s involvement in cases of fulminant and chronic non-A-E hepatitis, possibly related to genomic mutations which increase the pathogenesis of the virus. 33,34 All 5 patients with anti-HEV IgG recovered. Although we could not confirm HEV as the actual etiology, we identified a possible risk factor in at least 1 patient, who had returned from a trip to the Caribbean 30 days before the onset of symptoms.…”

Section: Discussionmentioning

confidence: 96%

Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: Etiology and natural history

Bahia¹,

Vitvitski

Andrade

et al. 1999

Hepatology

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In a 4-year follow-up study, patients with acute sporadic non-A, non-B (NANB) hepatitis were evaluated to determine the etiology and natural history of the disease. Acute hepatitis C virus (HCV) was detected in 13 of 43 (30%) of patients, anti-hepatitis E virus (HEV) IgG in 5 (12%), and 25 (58%) were considered non-A-E. The HCV RNA was detected in all HCV patients but none of the non-A-E cases. The initial clinical and biochemical presentation of the HCV and non-A-E cases was quite similar, although 2 of the non-A-E patients had severe disease. The 5 patients who were found to be anti-HEV IgG-reactive recovered within 6 months of follow-up. Of the 13 HCV cases, alanine transaminase (ALT) levels returned to normal in 7 (53.8%), while 6 (46.2%) continued to show abnormal ALT after 6 months of follow-up. However, 9 (69.2%) of them remained HCV-RNApositive, denoting virological/biochemical dissociation. Longterm follow-up showed a reappearance of HCV RNA in 2 of the 4 patients who were in virological remission performing 84% of chronicity rate. Acute non-A-E hepatitis patients were less likely to evolve toward chronicity, as compared with acute HCV cases (16% vs. 84%; P ‫؍‬ .0001). Only 4 (16%) of the non-A-E patients were hepatitis G virus (HGV)-RNA-positive. Concerning risk factors for acquiring parenterally transmitted viruses, tattooing was the only one that could be associated with HCV transmission (P ‫؍‬ .002). No risk factors could be identified for putative non-A-E virus transmission. Liver biopsies performed for chronic HCV patients showed a variable degree of inflammation, while the non-A-E patients presented less severe histological disease. (HEPATOLOGY 1999;30:289-293.)

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Section: Discussionmentioning

confidence: 96%

Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: Etiology and natural history

Bahia¹,

Vitvitski

Andrade

et al. 1999

Hepatology

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“…GBV-C anti-E2 antibodies seem to protect from GBV-C infection. Apart from a possible role in fulminant hepatitis, [25][26][27] previous studies have indicated a rather benign character of a GBV-C infection. 28,29 Our results indicate that GBV-C infection itself may not be harmful to humans, but the interaction with the immune system is important for viral clearance.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1998

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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. (HEPATOLOGY 1998;28:379-384.)

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“…1997). The association of HGV with hepatitis is suggested by prevalence studies (Yoshiba et al, 1995 ;Colombatto et al, 1996 ;Fiordalisi et al, 1996 ;Linnen et al, 1996 ;Tameda et al, 1996) and in one case by a prospective study of transfusion recipients (Linnen et al, 1996). However, more recent evidence suggests that HGV would probably account for only mild clinical disease at best Egawa et al, 1996 ;Masuko et al, 1996 ;Tanaka et al, 1996 ;Wang et al, 1996 ;Alter et al, 1997 a, b ;Bralet et al, 1997 ;Haydon et al, 1997 ;Wang & Jin, 1997).…”

Section: Introductionmentioning

confidence: 95%

“…It is now well-established that HGV is a transfusiontransmitted blood-borne virus highly prevalent around the world and that persistent infection with HGV is common (Aikawa et al, 1996 ;Egawa et al, 1996 ;Masuko et al, 1996 ;Nakatsuji et al, 1996 ;Stark et al, 1996 ;Tameda et al, 1996 ;Tsuda et al, 1996 ;Alter et al, 1997 a, b ;Brown et al, 1997 ;Dawson et al, 1997 ;Feucht et al, 1997 ;Kinoshita, et al, 1997 ;Theodore & Lemon, 1997 ;Wang & Jin, 1997 ;Wu et al, Author for correspondence : Dong-Yan Jin.…”

Section: Introductionmentioning

confidence: 99%

Identification of a single genotype of hepatitis G virus by comparison of one complete genome from a healthy carrier with eight from patients with hepatitis.

Wang

Hou²,

Jin³

1997

Journal of General Virology

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Different isolates of a putative hepatitis virus called hepatitis GB virus C or hepatitis G virus (HGV) have been cloned recently from patients with hepatitis. This virus has also been found commonly in healthy carriers. We have cloned and sequenced a complete HGV genome, designated HGVCN, from a healthy Chinese blood donor. HGVCN shares 85n8-90n0% nucleotide sequence identity and 95n4-97n5% amino acid identity with the eight available fulllength HGV genomes. Furthermore, the majority (82n8 %) of the nucleotide substitutions found in HGVCN were synonymous and a fairly uniform distribution of changes was found across the entire genome without identification of any hypervariable

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Infection with GB virus C (GBV-C) in patients with fulminant hepatitis

Cited by 45 publications

References 16 publications

Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: Etiology and natural history

Acute sporadic non-A, non-B hepatitis in Northeastern Brazil: Etiology and natural history

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

Identification of a single genotype of hepatitis G virus by comparison of one complete genome from a healthy carrier with eight from patients with hepatitis.

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