Background and Objectives: Two new flaviviruses, hepatitis G virus and GB v
irus type C (GBV-C), are possible causative agents for non-A-E hepatitis. I
n this study we established the prevalence of GBV-C markers in various popu
lation subsets in The Netherlands by assays for GBV-C antibodies and GBV-C
nucleic acid. Materials and Methods: We tested specimens from groups of pat
ients with hepatitis of various causes, intravenous drug users (IVDUs), and
blood donors for GBV-C RNA (LCx(R) GBV-C assay, Abbott Laboratories), and
for antibodies to the GBV-C envelope E2 protein (GBV-C anti-E2) with an enz
yme immunoassay (Abbott Laboratories). Patients and donors were represented
in one group only. Results: GBV-C RNA and GBV-C anti-E2 prevalence were, r
espectively, 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 (7
1%) among IVDUs, 1/34 (3%) and 2/34 (6%) among blood donors with indetermin
ate 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%) fi rst time blood donors. Conc
lusion: GBV-C infection appears not to be a major cause of non-A-E hepatiti
s 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 h
ave probably previously been exposed to GBV-C given the very high prevalenc
e of GBV-C anti-E2 (71%). Most persons with GBV-C markers are GBV-C RNA-neg
ative and anti-E2-confirmed positive, suggesting that GBV-C infection is tr
ansient.