GB Virus Type C Viremia and Envelope Antibodies among Population Subsets in The Netherlands

Abstract

Abstract Background and Objectives: Two new flaviviruses, hepatitis G virus and GB virus type C (GBV‐C), are possibele causative agents for non‐A‐E hepatitis. In this study we established the prevalence of GBV‐C markers in various population subsets in The Netherlands by assays for GBV‐C antibodies and GBV‐C nucleic acid. Materials and Methods: We tested specimens from groups of patients with hepatitis of various causes, intravenous drug users (IVDUs), and blood donors for GBV‐C BNA (LCx® GBV‐C assay, Abbott Laboratories), and for antibodies to the GBV‐C envelope E2 protein (GBV‐C anti‐E2) with an enzyme immunoassay (Abbott Laboratories). Patients and donors were represented in one group only. Results: GBV‐C RNA and GBV‐C anti‐E2 prevalence were, respectively, 2/34 (6%) and 3/34 (9%) among patients with non‐A‐E hepatitis, 2/10 (20%) and 0/10 (0%) among hepatitis B virus patients, 10/40 (25%) and 19/40 (48%) among hepatitis C virus (HCV) patients, 1/8 (13%) and 0/8 (0%) among patients with autoimmune hepatitis (AIH), 24/102 (24%) and 72/102 (71%) among IVDUs, 1/34 (3%) and 2/34 (6%) among blood donors with indeterminate anti‐HCV recombinant immunoblot assay reactivity, and 3/250 (1.2%) and 8/250 (3.2%) among first‐time blood donors. the profile of simultaneous GBV‐C RNA positivity plus GBV‐C anti‐E2 positivity was found in 2/40 (5%) HCV patients, 4/102 (4%) IVDUs, and 1/250 (0.4%) first time blood donors. Conclusion: GBV‐C infection appears not to be a major cause of non‐A‐E hepatitis and AIH, but is associated with parenteral risk. The prevalence of GBV‐C viremia in first time blood donors is higher than that of HCV (1.2 vs. 0.04%), but, GBV‐C viremia in IVDUs is lower than HCV (24 vs. 59%). Most IVDUs have probably previously been exposed to GBV‐C given the very high prevalence of GBV‐C anti‐E2 (71%). Most persons with GBV‐C markers are GBV‐C marker are GBV‐C RNA‐negative and anti‐E2 confirmed positive, suggesting that GBV‐C infection is transient.