J. T. Stapleton and others clear that neither virus was associated with a mild form of chronic hepatitis frequently observed in recipients of blood transfusions (Feinstone et al., 1975). Considerable research was directed towards identifying the causative agent of post-transfusion or ‘non-A, non-B’ hepatitis (Feinstone et al., 1975; Feinstone & Purcell, 1978; Prince et al., 1974), and well characterized human sera were shown to contain an infectious agent that caused chronic, relapsing and mild hepatitis in experimentally infected chimpanzees (Bradley et al., 1983). Using a molecular cloning approach, Choo et al. (1989) discovered an RNA virus in the serum and tissues of a chimpanzee experimentally inoculated with serum from an individual with chronic, non-A, non-B hepatitis (Choo et al., 1989). This virus was shown to be epidemiologically associated with non-A, non-B hepatitis (Kuo et al., 1989), and chimpanzee studies confirmed that the virus induced hepatitis (Bradley, 2000). The virus was called hepatitis C virus (HCV) and it is classified as the type species member of the genus Hepacivirus within the family Flaviviridae (Choo et al., 1989). In the process of studying non-A, non-B hepatitis, Dienhardt and colleagues obtained serum from a surgeon on day 3 of acute hepatitis (Deinhardt et al., 1967). This serum apparently induced hepatitis when inoculated into tamarins, a type of New World monkey (Saguinus labiatus). Passage of serum obtained from the inoculated animals at the time of hepatitis into new tamarins produced similar hepatitis both in newly inoculated tamarins and in other New World monkey species (Deinhardt et al., 1967). Based on the initials of the surgeon, the transmissible agent was called the ‘GB agent’, and this agent was studied extensively as a putative cause of non-A, non-B hepatitis (Deinhardt et al., 1967; Deinhardt & Deinhardt, 1984; Gust & Feinstone, 1988). In 1995, a group of investigators from Abbott Laboratories identified two viruses in the serum and liver of tamarins inoculated with the 11th tamarin passage of the GB agent (Simons et al., 1995b). These viruses were named GB virus A and B (GBV-A and GBV-B) due to the pedigree of the infectious serum (Simons et al., 1995b). Using degenerate primers to amplify related viral sequences in human serum samples, a third virus was identified and termed GBV-C (Simons et al., 1995a). Simultaneously, a research group at Genelabs identified novel RNA virus sequences in the serum of humans with non-A, non-B hepatitis, and called this virus hepatitis G virus (HGV) (Linnen et al., 1996). Subsequent analysis of the genome sequences of HGV and GBV-C revealed that they were minor variants of the same virus species, while GBV-A and GBV-B were distinct (Kim & Fry, 1997; Leary et al., 1996b; Muerhoff et al., 1995). All of the ‘GB’ viruses are distantly related to HCV (Linnen et al., 1996; Simons et al., 1995a, b) and based on their predicted genome structure and nucleotide sequence relation- ships, the three ‘GB’ viruses were classified as members of the family Flaviviridae (http://www.ncbi.nlm.nih.gov/ICTVdb/ index.htm). Phylogenetic analysis of conserved regions of translated sequences from the helicase and polymerase 234 domains revealed a closer relationship of HCV to GBV-B, while GBV-A and GBV-C/HGV form a separate cluster (Muerhoff et al., 1995; Simons et al., 1995a). GBV-B represented the true GB-agent. Although it apparently did not originate from the surgeon GB and does not infect humans or chimpanzees, it caused acute hepatitis in experimentally infected tamarins, including animals trans- fected intrahepatically with RNA transcripts of recombinant GBV-B (Bukh et al., 1999; Lanford et al., 2003; Martin et al., 2003; Nam et al., 2004). In contrast, GBV-A represented indigenous tamarin viruses not associated with hepatitis (Simons et al., 1995b), and a number of GBV-A-like agents were subsequently identified from New World monkeys (Bukh & Apgar, 1997; Leary et al., 1996a; Simons et al., 1995b). GBV-C was found to be a frequent human virus that was not associated with viral hepatitis (Alter, 1997; Alter et al., 1997a; Simons et al., 1995a). Recently, using unbiased, high-throughput pyrosequencing methods, a virus more distantly related to GBV-A, GBV-B and GBV-C/HGV was identified in serum samples obtained from Old World frugivorous bats (P. giganteus) in Bangladesh (Epstein et al., 2010). Two full-length sequences were generated that share approximately 50 % amino acid sequence identity with GBV-A and GBV-C/ HGV (Epstein et al., 2010). This novel virus was named GBV-D. For three reasons, we suggest that the current nomencla- ture assigned to the ‘GB’ viruses should be changed. Firstly, there is no evidence that the surgeon (GB) for whom these viruses are named was infected with GBV-A, GBV-B, GBV- C/HGV or GBV-D. Secondly, infections and susceptibility to GBV-A and GBV-B have subsequently been shown to be restricted to New World primates, and to date, GBV-D appears to be restricted to bats. Thus, it is highly unlikely that they originated from the surgeon ‘GB’. Finally, GBV- C/HGV does not cause hepatitis in humans. In this manuscript, we review the clinical and virological aspects of these viruses and re-examine their genetic relationships. Based on these observations we propose a change in nomenclature of GBV-A, GBV-C/HGV and GBV-D to better and more clearly describe these viruses. Since GBV-B represents what for years has been referred to as the GB- agent, and since the natural host(s) of this virus remain unknown, we at present propose to remove the ‘B’ designation and call the virus ‘GBV’, as it will be the only GB virus under the proposed classification system. Virology Epidemiology and transmission HCV and GBV-C/HGV infections occur worldwide (reviewed by Lauer & Walker, 2001; Stapleton, 2003). It has been estimated that perhaps as many as 3 % of the world’s population has been infected with HCV (The Global Burden of Disease Working Group, 2004). Frequencies of GBV-C/HGV infection are difficult to determine, but prevalence studies suggest that 1–4 % of Journal of General Virology 92