J. T. Stapleton and others Fig. 4. Proposed classification of GB viruses. GBV-B, a member of the genus Hepacivirus with type species HCV, would be renamed GB virus (GBV); this virus is the true GB agent causing acute hepatitis in experimentally infected tamarins. The new genus designation for GBV-A, GBV-C/HGV and GBV-D would be Pegivirus for persistent ‘GB’ or ‘G’ virus. GBV-A and GBV-A-like viruses would become simian Pegivirus (SPgV) and species- specific viruses would have the species name in subscripts. GBV- C (or HGV) would become the human Pegivirus (HPgV), GBV- Ccpz would become SPgVcpz, and GBV-D would become bat Pegivirus (BPgV). If BPgV isolates found in different bat species segregate by species as with SPgV, the host species will be identified as a subscript. Examples of other viruses within the family Flaviviridae are shown for comparison. Taxonomy of Viruses (ICTV) for consideration. We believe that this classification clarifies that these viruses share several biological features including similar phylogeny and genome structures, the ability to cause persistent infection in their respective hosts, and finally, that they do not cause hepatitis. If closely related viruses are identified in different host species, we recommend that they be designated by the host genus for the first initial, followed by PgV. These new designations will better clarify the relationships between the ‘GB’ agents and resolve confusion regarding their relationship to the surgeon ‘GB’. 242 Acknowledgements This work was supported in part by a Merit Review grant from the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development (J. T. S.), and a grant from the National Institutes of Health (RO1 AI-58740, J. T. S.). Jens Bukh is the recipient of a professorship at the University of Copenhagen with external funding from the Lundbeck Foundation. References Adams, N. J., Prescott, L. E., Jarvis, L. M., Lewis, J. C. M., McClure, M. O., Smith, D. B. & Simmonds, P. (1998). Detection in chimpanzees of a novel flavivirus related to GB virus-C/hepatitis G virus. J Gen Virol 79, 1871–1877. Agnello, V., Abel, G., Elfahal, M., Knight, G. B. & Zhang, X. (1999). Hepatitis C virus and other flaviviridae viruses enter cells via low density lipoprotein receptor. Proc Natl Acad Sci U S A 96, 12766– 12771. Alter, H. J. (1997). G-pers creepers, where’d you get those papers? A reassessment of the literature on the hepatitis G virus. Transfusion 37, 569–572. Alter, H. J., Nakatsuji, Y., Melpolder, J., Wages, J., Wesley, R., Shih, J. W.-K. & Kim, J. P. (1997a). The incidence of transfusion-associated hepatitis G virus infection and its relation to liver disease. N Engl J Med 336, 747–754. Alter, M. J., Gallagher, M., Morris, T. T., Moyer, L. A., Meeks, E. L., Krawczynski, K., Kim, J. P. & Margolis, H. S. (1997b). Acute non-A–E hepatitis in the United States and the role of hepatitis G virus infection. N Engl J Med 336, 741–746. Bakhshesh, M., Groppelli, E., Willcocks, M. M., Royall, E., Belsham, G. J. & Roberts, L. O. (2008). The picornavirus avian encephalomye- litis virus possesses a hepatitis C virus-like internal ribosome entry site element. J Virol 82, 1993–2003. Barnes, A., Allen, J. B., Klinzman, D., Zhang, W., Chaloner, K. & Stapleton, J. T. (2007). GBV-C persistence does not require CD4+ T cell preservation, and GBV-C viral load (VL) is weakly inversely related to HIV VL. 4th IAS Conference on HIV Pathogenesis, Treatment and Prevention. Sydney, Australia. Baumert, T. F., Welinitz, S., Aono, S., Satol, J., Herion, D., Tilman, J., Gerlach, R., Pape, G. R., Lau, J. Y. & other authors (2000). Antibodies against hepatitis C virus-like particles and viral clearance in acute and chronic hepatitis C. Hepatology 32, 610–617. Beames, B., Chavez, D., Guerra, B., Notvall, L., Brasky, K. M. & Lanford, R. E. (2000). Development of a primary tamarin hepatocyte culture system for GB virus-B: a surrogate model for hepatitis C virus. J Virol 74, 11764–11772. Beames, B., Chavez, D. & Lanford, R. E. (2001). GB virus B as a model for hepatitis C virus. ILAR J 42, 152–160. Berg, T., Muller, A. R., Platz, K. P., Hohne, M., Bechstein, W. O., Hopf, U., Wiedenmann, B., Neuhaus, P. & Schreier, E. (1999). Dynamics of GB virus C viremia early after orthotopic liver transplantation indicates extrahepatic tissues as the predominant site of GB virus C replication. Hepatology 29, 245–249. Birkenmeyer, L. G., Desai, S. M., Muerhoff, A. S., Leary, T. P., Simons, J. N., Montes, C. C. & Mushahwar, I. K. (1998). Isolation of a GB virus-related genome from a chimpanzee. J Med Virol 56, 44– 51. Blair, C. S., Davidson, F., Lycett, C., McDonald, D. M., Haydon, G. H., Yap, P. L., Hayes, P. C., Simmonds, P. & Gillon, J. (1998). Prevalence, incidence, and clinical characteristics of hepatitis G virus/GB virus C infection in Scottish blood donors. J Infect Dis 178, 1779–1782. Journal of General Virology 92