Molecular Cloning and Disease Association of Hepatitis G Virus: A Transfusion-Transmissible Agent

  title={Molecular Cloning and Disease Association of Hepatitis G Virus: A Transfusion-Transmissible Agent},
  author={Jeffrey M. Linnen and John M. Wages and Z Y Zhang-Keck and Kirk E. Fry and Krzysztof Krawczyński and Harvey J. Alter and Eugene Koonin and Margaret L. Gallagher and Miriam J. Alter and Stephanos J. Hadziyannis and Peter Karayiannis and Kevin Fung and Yoshiyuki Nakatsuji and J. Wai-Kuo Shih and L M Young and Michael Piatak and Cameron C. Hoover and John Fernandez and Stacie Chen and Jian-Chao Zou and T T Morris and Kenneth Craig Hyams and Susan L Ismay and Jeffrey D. Lifson and Georg Hess and Steven K. H. Foung and Howard Thomas and Daniel W. Bradley and Harold S. Margolis and Jungsuh P. Kim},
  pages={505 - 508}
An RNA virus, designated hepatitis G virus (HGV), was identified from the plasma of a patient with chronic hepatitis. Extension from an immunoreactive complementary DNA clone yielded the entire genome (9392 nucleotides) encoding a polyprotein of 2873 amino acids. The virus is closely related to GB virus C (GBV-C) and distantly related to hepatitis C virus, GBV-A, and GBV-B. HGV was associated with acute and chronic hepatitis. Persistent viremia was detected for up to 9 years in patients with… 
Hepatitis G virus: is it a hepatitis virus?
Although HGV appears to be a hepatotrophic virus, its role in independently causing acute and chronic liver diseases remains uncertain.
Identification, prevalence and aspects of molecular biology of hepatitis G virus
Construction of phylogenetic trees, and calculation of mean distances between possible subtypes, indicated one level of variation in NS‐3 sequences: the degree of variation between isolates was similar to that observed between HCV sub types, and no evidence for clustering of sequences into multiple genotypes was found.
Hepatitis C Virus: Worldwide Epidemic
This virus has remarkable genomic variability, hepatic and extra-hepatic replication in lymphocytes, bone marrow cells, adrenal gland and pancreas with inefficient replication.
Novel hepatitis agents: The significance of clinical and experimental studies. An overview
  • K. Krawczyński
  • Medicine, Biology
    Journal of gastroenterology and hepatology
  • 1997
The disease association of this new virus remains unconfirmed and its role in the etiology of acute and chronic hepatitis is unclear, but the experimental model of HGV/GBV‐C infection may define the biology of the virus replication.
GB Virus C/Hepatitis G Virus
Although the prevalence of HGV in association with acute and chronic hepatitis is higher than that in the general population, further prospective studies are needed to demonstrate its relative significance in causing hepatitis and other disease.
Effect of Hepatitis G Virus Infection on Chronic Hepatitis C
The role of HGV infection in patients with chronic hepatitis C, including patients treated with interferon, was analyzed, and the final diagnosis was established by consensus.
Emerging and re-emerging hepatitis viruses.
The presence of new hepatitis viruses was anticipated immediately after hepatitis A and B viruses were discovered and the main causative agent which is responsible for post-transfusion non-A, non-B hepatitis is hepatitis C virus (HCV).
Toward a surrogate model for hepatitis C virus: An infectious molecular clone of the GB virus-B hepatitis agent.
The development of severe hepatitis in both tamarins infected with the recombinant GBV-B virus provides formal proof that GBV -B is a true hepatitis virus.


Isolation of novel virus-like sequences associated with human hepatitis
The limited nucleotide sequence identity betweenGBV-A, GBV-B and HCV sequences suggests that a novel virus, tentatively named GB virus C, may be responsible for some cases of non-A/B/B, non-C/C/D/E hepatitis.
Hepatitis E virus: identification of type-common epitopes
The isolation, by serologic screening, of two cDNA clones derived from a fecal sample collected during a 1986 outbreak of ET-NANBH in Telixtac, Mexico represent the initial cloning of the Mexico strain of HEV.
An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis
Assays of ten blood transfusions in the United States that resulted in chronic NANBH revealed that there was at least one positive blood donor in nine of these cases and that all ten recipients seroconverted during their illnesses.
Isolation of the novel agent from human stool samples that is associated with sporadic non-A, non-B hepatitis
The results indicate that 27- to 37-nm virus like particles are responsible for sporadic non-A, non-B hepatitis in rhesus monkeys and were able to protect monkeys challenged with infectious stool extract.
Identification of two flavivirus-like genomes in the GB hepatitis agent.
Limited sequence identity with various isolates of hepatitis C virus and the relative positions of putative RNA helicases and RNA-dependent RNA polymerases in the predicted protein products of these molecules suggested that the GB agent contains two unique flavivirus-like genomes.
The natural history of community-acquired hepatitis C in the United States. The Sentinel Counties Chronic non-A, non-B Hepatitis Study Team.
Patients with community-acquired hepatitis C have a high rate of chronic hepatitis, and in most patients HCV infection seems to persist for at least several years, even in the absence of active liver disease.
Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection.
Patients with no history of transfusions were just as likely to be positive for antibody to hepatitis C virus as patients with transfusion-associated hepatitis, indicating that hepatitis Cirus is the major causative agent of all non-A, non-B hepatitis in the United States.
Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis.
It is concluded that hepatitis C virus is the predominant agent of transfusion-associated non-A, non-B hepatitis and that screening of donors for anti-HCV could prevent the majority of cases of the disease.
A second hepatitis C virus-encoded proteinase.
The 2/3 cleavage site is defined and evidence suggests that this cleavage is mediated by a second HCV-encoded proteinase, located between aa 827 and 1207, which should facilitate purification and further characterization of this enzyme.