Prevalence of GBV-C and hepatitis G virus variants in patients with fulminant hepatic failure in Japan

Background/Aims: Whether GB virus C and hepatitis G virus participate in fulminant hepatic failure is controversial. We studied the prevalence of the viral RNA in 48 patients. There were possible routes of infection, including blood transfusion, in 22 patients (group 1), and no risk factors in the other 26 (group 2). Methods: We assayed serum viral RNA with reverse transcription and nested polymerase chain reactions. Serum was obtained at admission, and after transfusion in group 2. Results: Five (10%) serum samples from group 1 at admission had viral RNA of the 5′-untranslated region, and three of these samples had viral RNA of the NS3/helicase region. All five patients had transfusions before sampling. Two (4%) samples from group 2 were positive by both tests only after transfusion. Of two patients, one with non-A–E fulminant hepatic failure survived. Her serum alanine aminotransferase did not increase further after transfusion, but did stay above the reference range during follow-up. The other patient, with infection with hepatitis B virus detected at admission, died. After transfusion, his alanine aminotransferase did not increase further. Partial nucleotide sequences of GB virus C and hepatitis G virus from three fulminant hepatic failure patients and five control patients with chronic hepatitis C were compared with published sequences. A viral variant causing fulminant hepatitis, suggested elsewhere, was not found, nor was all of a characteristic pattern of six mutations found elsewhere. Conclusions: GB virus C and hepatitis G virus may cause hepatitis, but probably not severe hepatitis such as fulminant hepatic failure.