As a result of the quest for yet unidentified viruses that cause human hepatitis, two novel flaviviruses were identified in the 1990s by two independent groups of researchers. GB virus C (GBV-C) was first identified in the sera from a West African population during an attempt to retrospectively track down the causative agent of an incident of acute hepatitis in a surgeon (whose initials were GB) (1). This new virus was however subsequently found to be unrelated to the episode of hepatitis experienced by the surgeon. Almost concurrently, hepatitis G virus (HGV) was independently cloned from the plasma of a patient with chronic hepatitis (2). Sequence comparisons of both viruses showed nucleotide and amino acid homologies of 86 and 95 per cent respectively, suggesting that they were isolates of one and the same virus (3). GBV-C/HGV infection is relatively common and has a worldwide distribution. GBV-C/HGV viraemia which is the presence of viral RNA in serum or plasma, reflects current infection. Clearance of viraemia is associated with antibody to the GBV-C/HGV envelope protein (E2) (4). Viraemia detection rates vary globally from 1 to 12.2 per cent in healthy blood donors (5,6). In this issue Kumar et al (7) report a 6 per cent viraemia rate among healthy blood donors, similar to an earlier report from this country (8). Exposure to GBV-C/HGV in a given population is the sum of the RNA and E2 antibody detection rates.