Screening for antibody to hepatitis C virus (anti-HCV) is usually carried out using microplate enzyme immunoassays (EIA). According to French Ministry of Health recommendations, any positive or dubious result has to be controlled on a second blood sample with a anti-HCV assay differing from the one used for the initial screening. This second test can either be another EIA or an immunoblot assay. The present article investigates the advantage of a strip immunoblot assay including 4-viral peptides (Riba-3) for this control. The use of Riba for the early diagnosis of hepatitis C infection and for the follow-up of infected patients is also evaluated. Riba can be used to assess false positive EIA reactions, for instance in cases with isolated antibody to NS5. From large clinical series, it appears that positive Riba serum profiles can be divided in two main groups: Strongly positive sera associate at least strong (3 or 4+) anti-capsid and anti-NS3 antibody reactivities. These profiles are often completed by anti-NS4 and/or anti-NS5 reactivities. Such profiles are associated with HCV viremia in about 90% of the cases. In this group, prevalence of viremia reaches 100% in patients with elevated level of serum alanin aminotransferase (ALT) and is slightly less frequent, 85%, in patients with normal level of ALT; Weakly positive sera lack either anti-capsid or anti-NS3 antibodies or exhibit only low reactivities (1+ or 2+) to these two antigens. These profiles can also be associated with antibodies to NS4 and/or NS5. Only 10% of patients with such Riba profiles are viremic. Weakly positive profile can be encountered during the early phase of HCV infection (recent seroconversion) or in patients who experience a favourable evolution of their HCV infection. Change of Riba profiles during follow-up provides fruitful information on recent seroconversions (increase in number and intensity of the reactivities). It can also help predict the outcome of HCV infection, a diminution of the intensity of Riba reactivities will confirm the extinction of viral replication.