Effect of Hepatitis G Virus Infection on Chronic Hepatitis C

Tanaka, Eiji; Alter, Harvey J.; Nakatsuji, Yoshiyuki; Shih, Jennifer; Kim, J. P.; Matsumoto, Akihiro; Kobayashi, Mamoru; Kiyosawa, Kendo

doi:10.7326/0003-4819-125-9-199611010-00007

Cited by 184 publications

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“…Molecular approaches similar to those employed for HCV led to the subsequent discovery of the hepatitis G virus (HGV) 16 and representational difference analysis (RDA) was used to discover another candidate non-A to E hepatitis agent that was designated GBV-C. 17 It was later shown that HGV and GBV-C were variants of the same agent 16 and that neither was a likely cause of unexplained hepatitis in humans. [18][19][20] Hence, the search for viral causes of cryptogenic liver disease continued. In 1997, Nishizawa et al 1 using RDA, found a novel agent in the serum of 3 of 5 patients with transfusion-associated hepatitis.…”

Section: Discussionmentioning

confidence: 99%

Transfusion-associated TT virus infection and its relationship to liver disease

et al. 1999

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TT virus (TTV) has been proposed as the causative agent of non-A to E hepatitis. We studied the association between TTV viremia and biochemical evidence of hepatitis in blood donors and prospectively-followed patients. TTV was found in 7.5% of 402 donors and in 11.0% of 347 patients before transfusion. The rate of new TTV infections was 4.7% in 127 nontransfused, and 26.4% in 182 transfused patients (P F .0001). The risk of infection increased with the number of units transfused (P F .0001). The rate of new TTV infections in 13 patients with non-A to E hepatitis (23.2%) was almost identical to the rate in 124 patients who were transfused, but did not develop hepatitis (21.8%). Of 45 patients with acute hepatitis C, 40.0% were simultaneously infected with TTV. TTV did not worsen the biochemical severity (mean ALT: 537 in TTV؉; 550 in TTV؊) or persistence of hepatitis C. In non-A to E cases, the mean ALT was 182 in those TTV-positive and 302 in TTV-negatives. No consistent relationship between alanine transaminase level and TTV DNA level was observed in 4 patients with long-term, sequential samples. Of 21 viremic subjects, 67% cleared TTV within 5 years (38% in 1 year); 33% were viremic throughout follow-up extending to 22 years. We conclude that TTV is a very common, often persistent infection that is transmitted by transfusion and by undefined nosocomial routes. We found no association between TTV and non-A to E hepatitis and no effect of TTV on the severity or duration of coexistent hepatitis C. TTV may not be a primary hepatitis virus. (HEPATOLOGY 1999;30:283-288.)TT virus (TTV) was discovered in 1997 by representational difference analysis of serial serum specimens from Japanese patients with transfusion-associated non-A to G hepatitis. 1 Because of a temporal association between TTV viremia and elevations in serum alanine transaminase (ALT) level in 3 of 5 patients studied, TTV was proposed as the causative agent of non-A to G hepatitis. 1 TTV was initially described as a single-stranded DNA virus of approximately 3,800 base pairs (bp) and considered to be a member of the parvovirus family. 2 A subsequent analysis suggested that it was a single-stranded circular DNA virus in the circovirus family. 3 These genomic characterizations have been questioned and, at present, the agent has not been definitively classified. Seroepidemiological studies have shown TTV to have global distribution. 2,[4][5][6] Although the potential association of TTV with cryptogenic hepatitis is intriguing, the pathological and clinical significance of this virus remains to be established. To assess more fully the etiological role of TTV in the causation of hepatitis, we determined the frequency of acute TTV infections and their relationship to hepatitis in a cohort of prospectivelyfollowed transfusion recipients who did and did not develop hepatitis and in nontransfused controls. Prevalence of the agent was assessed in blood donors and in patients at the time of hospital admission. MATERIALS AND METHODS Selection of Patients in Variou...

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Section: Discussionmentioning

confidence: 99%

Transfusion-associated TT virus infection and its relationship to liver disease

et al. 1999

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“…Hepatitis G virus was also detected in patients with no evidence of liver disease and without known risk factors, such as volunteer blood donors. Recent reports suggest that coinfection of HCV-infected patients with HGV does not influence the outcome of HCVrelated hepatitis or the response to interferon therapy (8,9). The aims of this study were (i) to study the prevalence of HGV infection in patients with chronic liver disease and in blood donors found positive for hepatitis B surface antigen (HBsAg) or anti-HCV; (ii) to examine whether HGV had an influence on HCV replication; and (iii) to analyze whether HGV/HCV coinfection influences the degree of liver disease.…”

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Influence of hepatitis G virus infection on liver disease

Diamantis

Koulentaki

Fasler‐Kan

et al. 1997

Eur. J. Clin. Microbiol. Infect. Dis.

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“…Although GBV-C/HGV was discovered as a putative agent of non-A-E hepatitis (2, 7) and GBV-C/ HGV RNA has been detected in the sera of patients with various liver diseases including fulminant hepatitis (39), chronic hepatitis C (1,4,34,38), and cirrhosis with or without hepatocellular carcinoma (13,14), recent works have shown that GBV-C/HGV may play a minor role in causing liver disease (2,3,10,11,22).…”

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Existence of Distinct GB Virus C/Hepatitis G Virus Variants with Different Tropism

Fogeda

López‐Alcorocho

Bartolomé

et al. 2000

J Virol

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To study the existence of GB virus C/hepatitis G virus (GBV-C/HGV) variants with different tropism, we have analyzed the heterogeneity and quasispecies composition of GBV-C/HGV isolated from in vitro-infected peripheral blood mononuclear cells (PBMC) and from sera, livers, and PBMC from two chronically infected patients. For this purpose, the GBV-C/HGV 5 noncoding region (5NCR) was amplified by reverse transcription-PCR and the amplified products were cloned and sequenced. These analyses showed that the master 5NCR sequences isolated from the in vitro-infected PBMC and from the PBMC isolated from the patient whose serum was used as the inoculum were identical but different from that of the inoculum. Furthermore, phylogenetic analysis revealed that all PBMC sequences grouped together into a branch which was separate from those of the inoculum. For one of the two chronically infected patients, all the sequences from the PBMC and one from the liver clustered into a single branch while the sequences from the serum and all the other liver sequences grouped together in the other branch. For the other patient, the sequences from the serum and PBMC and three sequences from the liver grouped together into one branch, while the remaining five sequences from the liver were separated in a different cluster. In conclusion, our results support the existence of different GBV-C/HGV variants with different tissue tropism.

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Effect of Hepatitis G Virus Infection on Chronic Hepatitis C

Cited by 184 publications

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Transfusion-associated TT virus infection and its relationship to liver disease

Transfusion-associated TT virus infection and its relationship to liver disease

Influence of hepatitis G virus infection on liver disease

Existence of Distinct GB Virus C/Hepatitis G Virus Variants with Different Tropism

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