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A new member of the Flaviviridae family has recently been cloned and completely sequenced. The new virus, tentatively named hepatitis G virus (HGV) and known to be closely related to GB virus C (GBV-C), is transmitted by blood and blood products, intravenous drug use and other behaviour associated with a high risk of parenteral exposure to blood. The association of the virus with hepatitis is demonstrated by the presence of raised liver transaminase (alanine aminotransferase, ALT) levels in patients infected with HGV in the absence of other identifiable causes of hepatitis. No patient sera from groups exposed to blood and blood products were found to be positive when tested for the presence of GBV-A or GBV-B sequences, two other recently described flaviviruses. Forty-five per cent of the HGV-infected patients investigated had normal ALT suggesting the existence of a normal carrier state. Persistent infection of up to 13 years duration was observed. Co-infection with hepatitis B or hepatitis C viruses (HBV and HCV) was commonly seen presumably because of shared risk factors. None of five patients with fulminant hepatic failure was positive for HGV infection. The virus is sensitive to interferon-alpha, but sustained responses were not seen with the treatment regimens used for HBV and HCV. Viral titres increased during immunosuppression following liver transplantation and the higher levels of viraemia were in one case accompanied by elavated ALT. Whether HGV (GBV-C) replicates in the liver in some or all cases remains to be established. Preliminary data suggest that it is present within peripheral blood lymphocytes.

Hepatitis G virus (HGV) was transmitted to 2 chimpanzees by inoculation with human plasma containing Ç108 genome equivalents (GE) of HGV. The infection was characterized by the late appearance (weeks 10 and 11 after inoculation [pi]) of viremia that persisted throughout the 120-week follow-up. Serum HGV titer increased steadily until it plateaued at 10 6 -10 7 GE/mL. However, despite this relatively high titer, neither of the chimpanzees developed hepatitis. The sequence of the viral genome, recovered from each chimpanzee at week 77 pi, differed from that of the inoculum by 5 nt (2 aa) and 27 nt (2 aa). Two more chimpanzees were inoculated with a first-passage plasma pool. The chimpanzee inoculated with Ç10 6.7 GE of HGV had viremia at week 1 pi. However, the viral titer increased with the same kinetics as observed in the first passage. The second chimpanzee inoculated with Ç10 4.7 GE of HGV had late appearance (week 7 pi) of viremia.Hepatitis G virus (HGV), also called GB virus C (GBV-C), Like other members of Flaviviridae, HGV has a positivesense, single-stranded RNA genome (Ç9.5 kb) consisting of a is a Flaviviridae-like agent that was discovered during searches for new human hepatitis agents was observed between HGV and members of the Flaviviridae family in the serine protease and RNA helicase regions of NS3 of nonviremic blood donors were positive for E2 antibodies, suggesting that most patients clear the virus [7,8] and that and the RNA-dependent RNA polymerase of NS5. Of interest, the ORF of HGV lacks sequences characteristic of a wellperhaps as many as 10% of the general population has been infected with HGV. Studies of HGV in transfusion-associated defined nucleocapsid protein. Also, HGV does not appear to have a poly (U) or poly (A) stretch in the 3 UTR. These and community-acquired hepatitis cases have not confirmed that HGV is an etiologic agent of hepatitis [5,6].properties are also characteristic of GBV-A, a viral agent identified in tamarins inoculated with the GB agent [10]. Genetically, HGV is most closely related to GBV-A, with an overall homology (aa) of Ç45% [1,3].

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