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Antibody Responses to Hepatitis C Virus by Second‐Generation Immunoassays in a Cohort of Patients with Bleeding Disorders
Author(s) -
Hatzakis A.,
Polychronaki H.,
Miriagou V.,
Yannitsiotis A.,
Chrispeels J.,
Troonen H.,
Karafoulidou A.,
Gialeraki A.,
Katsouyanni K.,
Mandalaki T.
Publication year - 1992
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/j.1423-0410.1992.tb05101.x
Subject(s) - seroconversion , medicine , hepatitis c virus , antibody , immunoassay , virology , hepatitis c , cohort , viral disease , virus , immunology , human immunodeficiency virus (hiv) , hepacivirus , flaviviridae , gastroenterology
The antibody responses and the prevalence patterns of antibodies to hepatitis C virus (anti‐HCV) in a cohort of patients (n = 210) with bleeding disorders were studied using a first‐generation and a second‐generation enzyme immunoassays (EIA‐1, EIA‐2) as well as a second‐generation recombinant immunoblot assay (RIBA‐2). The anti‐HCV prevalence as determined by EIA‐1 and EIA‐2 was 183/210 (87.1%) and 197/210 (93.8%), respectively (p = 0.0026). None of the 17 EIA‐2(+)/EIA‐1(‐) samples was scored nonreactive by RIBA‐2. At follow‐up, samples of 123 patients were tested. Twenty‐nine out of 111 patients reactive by EIA‐1 seroreverted according to EIA‐1 while the sero‐reversion rate with EIA‐2 was 0 out of the 121 (p<10 ‐8 ). The anti‐HCV prevalence by EIA‐2 was 150/154 (97.4%) in anti‐HIV‐1‐positive individuals and 47/56 (83.9%) in the anti‐HIV‐1‐negative ones (p = 0.001). However, high assay signals (OD 492 nm >2.0) were observed in 94/150 (62.7%) and 45/47 (95.7%) of the anti‐HIV‐1‐positive and ‐negative patients, respectively (p = 10 ‐5 ). The decreasing anti‐HCV reactivity among anti‐HIV‐1‐positive individuals was mainly due to diminishing c33c reactivity. Seroconversion to anti‐HCV was observed in 3/7 (42.9%) cases with acute icteric non‐A, non‐B hepatitis by both EIA‐1 and EIA‐2, while the remaining 4 cases had detectable levels of anti‐HCV 1–18 months before the acute episode.