title: IgG1 anti-P2 as a marker of response to interferon in patients with chronic hepatitis C.
abstract: To study the relations of antibody production to long-term outcomes after interferon (IFN) treatment in patients with chronic hepatitis C (CH-C), we used ELISA to measure the levels of antibodies against HCV core protein and peptides. Samples from 21 complete responders and 36 non-responders were collected before IFN therapy, soon after the end of IFN therapy and 6 months later. Using a set of 19 synthesized HCV core peptide antigens, we found that anti-P2 (11-25a.a.) was the most prevalent of all IgG antibodies (93%: 39/42). Among complete responders, IgG1 anti-P2 levels had fallen by the end of IFN therapy (from 79.8 +/- 60.4-46.1 +/- 44.2: P < 0.01), and were lower still 6 months after the end of IFN therapy (31.0 +/- 35.2: P < 0.001); this change was the greatest of all antibodies studied. Among the non-responders, there was no change within the follow-up period. Soon after the end of IFN therapy, IgG1 anti-P2 levels were more than 30% lower than the initial value in more than two-thirds of the complete responders, but in only one-third of the non-responders (14/20 vs. 8/25: P < 0.05). Six months after the end of IFN therapy, IgG1 anti-P2 levels were more than 30% lower than the initial value in more than 85% of the complete responders, but in only 12% of the non-responders (17/20 vs. 3/25: P < 0.001). In conclusion, the changes in levels of IgG1 anti-P2 paralleled the activity of chronic hepatitis C after IFN therapy, and IgG1 anti-P2 levels may be markers of the efficacy of IFN therapy.
authors.affiliation: First Department of Internal Medicine, University of Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hirayama
authors.forename: T
authors.initials: T
authors.lastname: Maruyama
authors.forename: H
authors.initials: H
authors.lastname: Mitsui
authors.forename: H
authors.initials: H
authors.lastname: Maekawa
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: N
authors.initials: N
authors.lastname: Hashimoto
authors.forename: K
authors.initials: K
authors.lastname: Koike
authors.forename: S
authors.initials: S
authors.lastname: Kimura
authors.forename: K
authors.initials: K
authors.lastname: Yasuda
authors.forename: S
authors.initials: S
authors.lastname: Iino
authors.forename: J
authors.initials: J
authors.lastname: Green
mesh_terms: D000328:Adult; D000368:Aged; D001667:Binding, Competitive; D015415:Biomarkers / Q000032:analysis; D000939:Epitopes / Q000276:immunology; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D018937:Hepatitis C Antibodies / Q000096:biosynthesis*; D018936:Hepatitis C Antigens / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis*; D007372:Interferons / Q000627:therapeutic use*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000276:immunology; D012367:RNA, Viral / Q000097:blood; D016896:Treatment Outcome; D014758:Viral Core Proteins / Q000276:immunology*
chemical_list: D015415:Biomarkers; D000939:Epitopes; D018937:Hepatitis C Antibodies; D018936:Hepatitis C Antigens; D007074:Immunoglobulin G; D010455:Peptides; D012367:RNA, Viral; D014758:Viral Core Proteins; C069130:nucleocapsid protein, Hepatitis C virus; D007372:Interferons