Does GB virus C (‘hepatitis G virus’) threaten the safety of our blood supply?

Molecular ‘fishing’ for viruses has now become a scientifically fashionable pastime. Following the striking success of Chiron Corporation in identifying hepatitis C virus (the causative agent of the majority of non‐A, non‐B hepatitis cases) by cloning techniques (Choo et al ., 1989) two companies have independently cloned a distinct flavivirus‐like virus, itself related to HCV. This brief editorial is not to discuss the scientifically elegant molecular manipulations that led to the cloning of this newly recognized virus: this is briefly reviewed by Karayiannis & Thomas (1996). Suffice to say the GBV‐C agent discovered at Abbott Laboratories (Simons et al. , 1995) was identified in human sera that reacted with two similar viruses (GBV‐A and GBV‐B). These had been cloned from serum of a tamarin inoculated with the GB agent derived from a surgeon who developed acute hepatitis 30 years ago. HGV was cloned by Genelabs Technologies (Linnen et al ., 1996) from the plasma of a patient with chronic hepatitis, co‐infected with HCV. Both GBV‐C and HGV are single positive‐stranded RNA viruses of ∼9400 nucleotides. Their genomic organization is consistent with the Flaviviridae; they have 25% nucleotide homology with HCV. GBV‐C and HGV are different isolates of the same virus (Masuko et al. , 1996) showing 86% nucleotide homology and 96% amino acid similarity.