To the Editor:
GB virus C (GBV-C) and hepatitis G virus (HGV) are recently discovered RNA viruses that infect humans. Because GBV-C and HGV are most likely isolates of the same virus, the GBV-C nomenclature will be used throughout this letter. GBV-C seems to cause hepatitis unrelated to infection with hepatitis A, B, C, D, or E viruses.1 It has been reported that GBV-C infection may be linked to fulminant hepatitis.2 3 Therefore, in a retrospective study, we investigated 109 patients (41 women and 68 men; median age, 49 years) who underwent liver transplantation between 1992 and 1996. Seventeen (15.6%) of them had a history of fulminant hepatitis, 11 of unknown etiology, 5 of hepatitis B virus (HBV) infection, and 1 of hepatitis A virus (HAV) infection. The other 92 (84.4%) patients had liver cirrhosis due to autoimmune hepatitis (27 [24.8%]), chronic hepatitis C virus (HCV) infection (27 [24.8%]), chronic HBV infection (11 [10.1%]), HBV and hepatitis D virus (HDV) infection (4 [3.7%]), alcohol abuse (15 [13.8%]), unknown etiology (6 [5.5%]), or other (2 [1.8%]). GBV-C infection was investigated by reverse transcription-polymerase chain reaction (RT-PCR) using primers of the helicase-like region. At the time of liver transplantation, 7 (6.4%) of the 109 patients had detectable GBV-C viremia. Of these 7 patients, 4 patients had liver cirrhosis due to alcohol abuse, 2 patients had autoimmune hepatitis, and 1 patient had a cryptogenic cirrhosis. None of the 17 patients with fulminant hepatitis had detectable GBV-C viremia before or at the time of transplantation. Postoperatively, the 7 GBV-C–infected patients and additionally 42 patients (38.5%) had detectable viremia in sera drawn between days 6 and 14 after transplantation. These 49 patients showed a persistent GBV-C viremia during follow-up between 5 months and 4 years. The other 60 patients remained negative in GBV-C PCR.
One important route of GBV-C transmission is blood products (blood plasma and erythrocyte and thrombocyte concentrates).4 Therefore, we examined the number of blood products administered to these patients in connection with liver transplantation. We did not find a significant difference between the number of blood products administered to the 42 patients who acquired GBV-C infection perioperatively (median, 142 U) and the 60 patients without GBV-C infection (median, 137.5 U).
From our results we conclude that GBV-C infection is not linked to fulminant hepatitis. Our data further show that patients who undergo liver transplantation are at high risk for acquiring GBV-C infection. The prevalence after transplantation was 41.2%, in contrast to 6.4% before transplantation. Transfusion-transmitted GBV-C infection has to be assumed due to the great number (median, 140 U) required for liver transplantation. This is in agreement with previously published data in patients with hematologic malignancy.5 Clinical studies are already in progress to evaluate the clinical impact of GBV-C infection in liver transplant recipients.
