Hepatitis G Infection in Drug Abusers with Chronic Hepatitis C

Aikawa, Tatsuya; Sugai, Yoshiki; Okamoto, Hiroaki

doi:10.1056/nejm199601183340316

Cited by 201 publications

(99 citation statements)

References 4 publications

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“…The data obtained up to the present indicate that the virus can persistently infect patients on maintenance haemodialysis for 16 years or longer (Masuko et al, 1996), and is transmitted by transfusion and intravenous drugs (Aikawa et al, 1996 ;Linnen et al, 1996 ;Masuko et al, 1996 ;Schmidt et al, 1996). Remarkably, the infection with GBV-C\HGV is prevalent in carriers of HCV (Aikawa et al, 1996 ;Egawa et al, 1996 ;Linnen et al, 1996 ;Masuko et al, 1996), indicating a common route of transmission or a possible synergism of the two viruses. Although persistent infection with GBV-C does not seem to be associated with significant hepatic injuries (Masuko et al, 1996), GBV-C RNA has been reported in some patients with fulminant non-A to E hepatitis (Yoshiba et al, 1995).…”

Section: Introductionmentioning

confidence: 84%

The entire nucleotide sequences of two GB virus C/hepatitis G virus isolates of distinct genotypes from Japan.

Okamoto

Nakao

Inoue

et al. 1997

Journal of General Virology

100

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Recently, putative viral agents responsible for human non-A to E hepatitis have been independently reported by two groups of investigators and designated GB virus C (GBV-C) and hepatitis G virus (HGV), respectively. The entire nucleotide sequences were determined for two viral genomes isolated from Japanese blood donors with GBV-C RNA. One of them (GT230) had a total genomic length of 9390 nucleotides (nt) with 5h and 3h untranslated regions of 551 and 313 nt, while the other (GT110) had genomic lengths of 9395, 281 and 315 nt, respectively. They both had a single long open reading frame, encoding 2842 amino acids (aa) in GT230 and 2933 aa in GT110. Surprisingly, they both lacked a clearly identifiable core gene, and possessed the E1/E2 gene with only four potential

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Section: Introductionmentioning

confidence: 84%

The entire nucleotide sequences of two GB virus C/hepatitis G virus isolates of distinct genotypes from Japan.

Okamoto

Nakao

Inoue

et al. 1997

Journal of General Virology

100

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“…Fax: +81-52-852-0849. E-mail : mizokami@med.nagoya-cu.ac.jp venous drug users [3,4]. Comparison of the nucleotide and the deduced amino acid sequences showed good homology between these viruses.…”

Section: Introductionmentioning

confidence: 98%

Three different GB virus C/hepatitis G virus genotypes

et al. 1997

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The 5'-untranslated region (5'-UTR) sequences of 33 GB virus C/hepatitis G virus (GBV-C/HGV) obtained from different geographic areas were determined through reversetranscription polymerase chain reaction and dideoxy chain termination sequencing, the alignment of sequences, the estimation of the number of nucleotide substitution per site, and construction of phylogenetic trees. The 5'-UTR of GBV-HGV was found to be heterogeneous, with 70.9-99.5% homology. Three distinct phylogenetic branches were observed consistently in all phylogenetic trees. GBV-C is the prototype for one, HGV for another, and there is a new branch which consisted of GBV-C/HGV isolates from Asia. Genotype-specific restriction sites for the restriction enzymes, ScrFI and BsmFI, were identified, and a simple restriction fragment polymorphism analysis was developed for genotyping. These data provide evidence that GBV-C/HGV consists of three different genotypes. Our simple genotyping assay will also provide a tool for epidemiological studies of GBV-C/HGV infection. © 1997 Federation of European Biochemical Societies.

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“…[1][2][3] The virus has been shown to be transmitted via parenterally administered blood or blood products. 4 In Japan the prevalence is estimated at 1.1% in voluntary donors without any markers of HCV or HBV infection. 5 There are many factors and pathologic conditions known to cause liver dysfunction after BMT, including drug-related toxicity, hepatic veno-occlusive disease (VOD), GVHD and viral hepatitis, due to infection with cytomegalovirus, herpes simplex virus, varicella zoster, adenovirus, hepatitis C virus (HCV) and hepatitis B virus (HBV).…”

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confidence: 99%

Long-term liver function of recipients with hepatitis G virus infection after bone marrow transplantation

Maruta

Tanabe

Hashimoto

et al. 1999

Bone Marrow Transplant

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Summary:To clarify the role of hepatitis G virus (HGV) infection in liver dysfunction following allogeneic BMT, we examined cryopreserved serum samples from 33 patients who had a history of blood transfusions before BMT and whose serum samples had been stored periodically, before BMT, on day 100, and thereafter for the presence of HGV-RNA and hepatitis C virus (HCV)-RNA by reverse transcription polymerase chain reaction. Nineteen patients (58%) out of 33 were positive for HGV-RNA before BMT and 10 for HCV-RNA. All patients positive for HCV-RNA were also positive for HGV-RNA. Patients were divided into three groups according to their viral status before BMT; namely, the G؉C؉ group (n = 10), the G؉C؊ group (n = 9) and the G؊C؊ group (n = 14). Two patients in the G؊C؊ group became positive for HGV-RNA after BMT. One patient in the G؉C؊ group suffered an acute exacerbation of hepatitis, with GPT levels reaching over 1000 IU/l, 2 and 3 years after BMT, showing quite a different clinical course from those in the G؉C؊ group. Excluding these three patients, GPT levels of the patients in the G؉C؉ group were significantly higher after day 100 and remained higher than those of patients in the G؉C؊ and G؊C؊ groups for at least 4 years. There were no significant differences in post-transplant GPT levels between the G؉C؊ group and the G؊C؊ group at any time point. Of the seven patients followed-up for 5 to 10 years, three patients became HGV-RNA-negative, while four remained positive. In the absence of HCV co-infection, the behavior of GPT values post transplant in patients with HGV infection did not differ from those without HGV infection. With respect to the patient who was G؉C؊ and showed high values of GPT 2 and 3 years post transplant, we suspect that his liver dysfunction might have been caused by some unknown virus or etiology. Keywords: GBV-C; HGV; BMT; liver function Correspondence: A Maruta, Department of Hematology/Chemotherapy, Kanagawa Cancer Center, 1-1-2 Nakao, Asahi-ku, Yokohama 241-0815, Japan Received 6 November 1998; accepted 15 March 1999Two hepatitis-associated viruses, GB virus C (GBV-C) and hepatitis G virus (HGV), were identified in 1995 and in 1996. 1,2 These two viruses were found to show a 95% nucleotide homology, which was thought to indicate that they were isolates of the same virus, members of the Flaviviridae family.

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Hepatitis G Infection in Drug Abusers with Chronic Hepatitis C

Cited by 201 publications

References 4 publications

The entire nucleotide sequences of two GB virus C/hepatitis G virus isolates of distinct genotypes from Japan.

The entire nucleotide sequences of two GB virus C/hepatitis G virus isolates of distinct genotypes from Japan.

Three different GB virus C/hepatitis G virus genotypes

Long-term liver function of recipients with hepatitis G virus infection after bone marrow transplantation

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