GB Virus C/Hepatitis G Virus Isolates in Japanese Haemophiliacs and their Origins

1998 ◽  
Vol 80 (08) ◽  
pp. 242-245 ◽  
Author(s):  
Yoshihide Fukuda ◽  
Tetsuo Hayakawa ◽  
Junki Takamatsu ◽  
Hidehiko Saito ◽  
Hiroaki Okamoto ◽  
...  
Keyword(s):  
Sequence Similarity ◽  
West African ◽  
Blood Products ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Route Of Transmission ◽  
Polymerase Chain ◽  
Hepatitis G ◽  
Virus C ◽  
Virus Isolates

SummaryJapanese haemophiliacs have been at high risk for infection with parenterally-transmissible viruses through the use of blood products, especially imported ones. Recently, novel transfusion-transmissible virus, GB virus C (GBV-C)/hepatitis G virus (HGV) were isolated. We investigated the origin and route of transmission of GBV-C/HGV isolates in haemophiliacs in Japan. GBV-C/HGV RNA was measured by nested reverse transcription polymerase chain reaction in 91 Japanese haemophiliacs. Phylogenetic analysis and genotypic grouping of GBV-C/HGV isolates in Japanese haemophiliacs were performed based on sequences in the 5’ untranslated region, and the characteristics were compared with those of reported isolates. GBV-C/HGV infection was present in 19 of 91 haemophiliacs (20.9%). Sequence analysis showed that 15 of the 19 isolates (78.9%) showed sequence similarity to a group in which mainly West African isolates have been reported. The other 4 isolates (21.1%) showed sequence similarity to Asian isolates. None of the GBV-C/HGV isolates showed sequences similar to those generally found in isolates from USA and Europe. The majority of GBV-C/HGV isolates found in Japanese haemophiliacs who are considered to have been infected by imported blood products were similar to those detected in West Africa.

scholarly journals Relation between GB virus C/hepatitis G virus and fulminant hepatic failure may be secondary to treatment with contaminated blood and/or blood products

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 274-278 ◽  
Author(s):  
R Halasz ◽  
L Barkholt ◽  
C Lara ◽  
C Hultgren ◽  
Y Ando ◽  
...  
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Healthy Subjects ◽  
Blood Products ◽  
Serum Samples ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Hepatitis G ◽  
Virus C ◽  
Contaminated Blood

BackgroundThe role of the recently discovered GB virus C (GBV-C)/hepatitis G virus in fulminant hepatic failure (FHF) has been debated. Although GBV-C RNA has been detected in many cases of FHF, recent data suggest that the relation between GBV-C and FHF may be accidental.AimsTo retrospectively investigate the possible relation between the presence of GBV-C markers (RNA or antibodies to the GBV-C envelope 2 (E2) glycoprotein) and FHF.MethodsThe presence of GBV-C RNA was determined in serum samples from 58 patients diagnosed with FHF using a reverse transcriptase polymerase chain reaction. Amplified genetic fragments were directly sequenced by the dideoxy chain termination method. Antibodies to GBV-C in serum samples were detected by enzyme immunoassay based on a recombinant GBV-C E2 protein.ResultsNine (16%) patients with FHF had GBV-C RNA and 14 (24%) had GBV-C E2 antibodies, which are higher frequencies than in healthy subjects (p<0.01 and p<0.05 respectively). Seven of ten patients with GBV-C markers during FHF tested negative for these markers before therapy with blood and/or blood products. Sequence analysis of the GBV-C NS3 region fragments of six FHF patients showed no common sequence pattern or motif.ConclusionsThe frequencies of both GBV-C RNA and antibodies are higher in patients with FHF than in healthy subjects. However, these increased frequencies may in many cases be explained by the use of contaminated blood and/or blood products given as therapy.

Detection of GB Virus-C/Hepatitis G Virus RNA in Serum by Reverse Transcription Polymerase Chain Reaction

1997 ◽  
Vol 52 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Bhavna Bhardwaj ◽  
KePing Qian ◽  
Jill Detmer ◽  
Masashi Mizokami ◽  
Janice A. Kolberg ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Reverse Transcription ◽  
Chain Reaction ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Virus Rna ◽  
Polymerase Chain ◽  
Hepatitis G ◽  
Virus C

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

1997 ◽  
Vol 78 (4) ◽  
pp. 737-745 ◽  
Author(s):  
H Okamoto ◽  
H Iizuka ◽  
F Tsuda ◽  
Y Miyakawa ◽  
M Mayumi ◽  
...  
Keyword(s):  
Nucleotide Sequences ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Hepatitis G ◽  
Virus C ◽  
Virus Isolates

scholarly journals The Incidence and Natural Course of Transfusion-Associated GB Virus C/Hepatitis G Virus Infection in a Cohort of Thalassemic Patients

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 774-777 ◽  
Author(s):  
Daniele Prati ◽  
Alberto Zanella ◽  
Patrizia Bosoni ◽  
Paolo Rebulla ◽  
Elena Farma ◽  
...  
Keyword(s):  
Natural Course ◽  
Chain Reaction ◽  
Serum Samples ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Polymerase Chain ◽  
Hepatitis G ◽  
Virus C ◽  
A Prospective Study

To evaluate the risk of transmitting blood-borne GB virus C/hepatitis G virus (GBV-C/HGV) and to define the natural course of infection, we performed a prospective study in a cohort of multitransfused β-thalassemics during a 6-year follow-up period. We analyzed serum samples of 150 patients collected at 3-year intervals from 1990 to 1996. GBV-C/HGV RNA was determined by reverse transcriptase-polymerase chain reaction and antibodies to E2-protein by an enzyme immunoassay. At baseline, 14.5% of patients had viremia and 18.5% anti-E2. None of the patients with anti-E2 in 1990 subsequently became viremic. Of the 100 GBV-C/HGV RNA−, anti-E2− patients, 10 acquired infection during follow-up, as indicated by positivity of GBV-C/HGV RNA (n = 2), anti-E2 (n = 7), or both markers (n = 1) in 1996. The incidence was 1.7 per 100 person-years (95% confidence interval [CI], 0.8 to 3). Since approximately 19,000 blood units were transfused to these patients during follow-up, the risk of infection was 5.3 in 10,000 units (95% CI, 2 to 8.5). Six of 22 viremic patients cleared the virus during follow-up; 4 of them became anti-E2+. Twelve of 28 patients lost anti-E2 reactivity during follow-up. In conclusion, more than 25% of infections resolve within 6 years; the presence of anti-E2 seems to be protective against infection. Anti-E2 reactivity may decrease with time.

scholarly journals The Incidence and Natural Course of Transfusion-Associated GB Virus C/Hepatitis G Virus Infection in a Cohort of Thalassemic Patients

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 774-777 ◽  
Author(s):  
Daniele Prati ◽  
Alberto Zanella ◽  
Patrizia Bosoni ◽  
Paolo Rebulla ◽  
Elena Farma ◽  
...  
Keyword(s):  
Natural Course ◽  
Chain Reaction ◽  
Serum Samples ◽  
Hepatitis G Virus ◽  
Gb Virus C ◽  
Polymerase Chain ◽  
Hepatitis G ◽  
Virus C ◽  
A Prospective Study

Abstract To evaluate the risk of transmitting blood-borne GB virus C/hepatitis G virus (GBV-C/HGV) and to define the natural course of infection, we performed a prospective study in a cohort of multitransfused β-thalassemics during a 6-year follow-up period. We analyzed serum samples of 150 patients collected at 3-year intervals from 1990 to 1996. GBV-C/HGV RNA was determined by reverse transcriptase-polymerase chain reaction and antibodies to E2-protein by an enzyme immunoassay. At baseline, 14.5% of patients had viremia and 18.5% anti-E2. None of the patients with anti-E2 in 1990 subsequently became viremic. Of the 100 GBV-C/HGV RNA−, anti-E2− patients, 10 acquired infection during follow-up, as indicated by positivity of GBV-C/HGV RNA (n = 2), anti-E2 (n = 7), or both markers (n = 1) in 1996. The incidence was 1.7 per 100 person-years (95% confidence interval [CI], 0.8 to 3). Since approximately 19,000 blood units were transfused to these patients during follow-up, the risk of infection was 5.3 in 10,000 units (95% CI, 2 to 8.5). Six of 22 viremic patients cleared the virus during follow-up; 4 of them became anti-E2+. Twelve of 28 patients lost anti-E2 reactivity during follow-up. In conclusion, more than 25% of infections resolve within 6 years; the presence of anti-E2 seems to be protective against infection. Anti-E2 reactivity may decrease with time.

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