The GB Viruses: An Update of Their Biology, Molecular Virology and Significance

Abstract

In the quest to identify further viruses associated with hepatitis, three new viruses were cloned and assigned to the Flaviviridae family in the mid‐1990s. These were named the GB virus A (GBV‐A), GBV‐B and GBV‐C/hepatitis G virus (HGV). A more recent member is GBV‐D. Of these, GBV‐B, which is not a human pathogen, is associated with hepatitis in tamarins ( Saguinus sp). GBV‐A, ‐C/HGV and ‐D, in turn, infect primates, humans and frugivorous bats. These three viruses, unlike GBV‐B, are characterised by the lack of an identifiable core protein and do not appear to be associated with any signs and symptoms of disease. Moreover, the liver does not appear to be the primary site of replication for GBV‐A and GBV‐C/HGV. Instead, the lymphoid system seems to be their primary target. The current review deals with what is known of the natural history, virology and molecular biology of these viruses. Key Concepts: GBV‐A, GBV‐B, GBV‐C/HGV and GBV‐D are members of the Flaviviridae family. GBV‐B causes hepatitis only in tamarins ( Saguinus sp). GBV‐A, ‐C/HGV and ‐D are not associated with hepatitis. GBV‐A and ‐C/HGV appear to replicate primarily in lymphocytes. GBV‐A, ‐C/HGV and ‐D do not have an identifiable core‐encoding region in their genome. GBV‐A and ‐C/HGV cause persistent infection. Loss of GBV‐C/HGV viraemia is associated with the development of anti‐E2 antibodies.