The clinical significance of HGV infection is uncertain.
Although hepatitis G virus infection (HGV) is usually
Hepatitis G viremia has been documented in patients with asymptomatic, it has been associated with mild hepatic injury.
acute hepatitis 1,6,7 and can persist for years, 1,5-7 although ami-Whether hepatitis G co-infection alters the natural history of notransferase levels appear to normalize in many patients other viral hepatitis infections remains to be determined. In with chronic infection. 6,7 HGV RNA has been identified in the present study, we investigated whether hepatitis G impatients with fulminant hepatic failure 8,9 but it is not known pacts on the time to recurrent hepatitis or on the time to whether HGV was the proximate cause of fulminant hepatic progression to fibrosis in hepatitis C-infected patients who failure in these cases. HGV also has been found to be more undergo liver transplantation. Forty-five liver transplantation prevalent in patients with cryptogenic cirrhosis (7% to recipients with persistent hepatitis C viremia by polymerase 20%), 10,11 than in healthy blood donors (1% to 2%). However, chain reaction (PCR) were evaluated. Stored sera obtained in these studies it was not evident whether HGV infection before and after liver transplantation was tested for HGV RNA preceded the development of advanced liver disease. In a by reverse transcriptase (RT)-PCR using primers to the 5
further study, all HGV-infected patients with cryptogenic region of the HGV genome. A median of eight serial liver cirrhosis received blood transfusions after, but not before, biopsy specimens were reviewed per patient. The prevalence the diagnosis of cirrhosis. 12 of HGV co-infection was 21% before transplantation and 22%
To date, it is not clear whether HGV causes recurrent liver following transplantation. During a median follow-up of 29 disease after transplantation. In one study, HGV RNA was months, 78% (35/45) of patients with hepatitis C viremia detected in 31% of patients with unexplained hepatitis after developed histological features of recurrent hepatitis. Fiftyliver transplantation, although a similar proportion of paone percent (23/45) progressed to fibrous portal expansion tients with unexplained hepatitis did not have hepatitis G and 16% (7/45) developed bridging fibrosis. Comparisons of viremia. 11 In another report, two patients with HGV infection patients with and without hepatitis G co-infection following before liver transplantation did not develop histological evitransplantation showed no significant difference in time to dence of hepatitis after transplantation. 13 Attention also has recurrent hepatitis, fibrous portal expansion, bridging fibrofocused on whether the natural history of hepatitis B virussis, or of allograft or patient survival. In conclusion, hepatitis and hepatitis C virus (HCV)-related liver disease are altered G co-infection does not seem to impact on the time to recurby HGV co-infection. Studies of patients who have not underrent hepatitis C or progression of hepatitis C-related histogone liver transplantation suggest that HGV infection does logical injury after liver transplantation. (HEPATOLOGY 1997; not alter the clinical course of acute or chronic hepatitis 26:432-436.)
C. 6,7 With regard to liver transplantation, preliminary data indicate that HGV does not significantly affect the develop-The hepatitis G virus (HGV) is a newly identified RNA ment of recurrent hepatitis B infection. 14 In one report, HGV virus 1 with an estimated prevalence of 1% to 2% in volunteer co-infection was not associated with disease severity in liver blood donors in the United States. 1,2 Sequence analysis sugtransplantation recipients with recurrent hepatitis C. 15 gests that HGV and the recently described hepatitis GB virus Whether HGV acts synergistically with HCV to cause hepa-C 3 represent isolates of the same virus. These seem to be tocellular injury in transplantation recipients, is particularly related to the GB viruses A and B that have been identified interesting because the variable course of recurrent hepatitis in Tamarins but not in humans. 2,4 Epidemiological data sug-C after transplantation has not been fully explained. Hepatigest that HGV may be spread through parenteral routes such tis C viremia tends to persist following liver transplantaas blood transfusion and intravenous drug use. [5][6][7] tion, [16][17][18][19] although a proportion of patients remain free of recurrent hepatitis with up to 4 years of follow-up. 17 Among those who develop recurrent hepatitis, pathological changes Abbreviations: HGV, hepatitis G virus; HCV, hepatitis C virus; PCR, polymerase range from mild inflammation to aggressive disease with prochain reaction.
gression to cirrhosis and liver failure. While genotype, [20][21][22]