title: Significance of anti-interferon-alpha2 and sICAM-1 activities in the sera of viral hepatitis B and C patients treated with human recombinant interferon-alpha2.
abstract: In this study the presence of an IFN-binding activity in the sera of patients with chronic viral hepatitis B or C treated with rIFN-alpha2 was screened by a radioimmune assay (RIA) using radiolabeled rIFN-alpha2. Incidence of an anti-IFN activitywas compared with hepatitis B virus (HBV) or hepatitis C virus (HCV) serum markers as hepatitis B s antigen (HBsAg), hepatitis B e antigen (HBeAg), antibodies to HBsAg (anti-HBsAg), antibodies to HBeAg (anti-HBeAg), seroconversion, HBV DNA, HCV RNA, and serum soluble intracellular adhesion molecule I (sICAM). Injections (intramuscular) of rIFN-alpha2 caused an anti-rIFN activity formation in 8 (27.6%) of 29 patients with chronic active hepatitis B (CAH-B) and in 8 (30.8%) of 26 patients with chronic active hepatitis C (CAH-C). The presence of the anti-rIFN activity in CAH-B patients correlated frequently with the persistence of HBsAg, HBeAg and HBV-DNA, while its absence was often accompanied by the anti-HBeAg and anti-HBsAg seroconversion, respectively, and HBV-DNA negativity. In two CAH-C patients who became HCV RNA-negative no anti-IFN activity was found. Levels of serum sICAM-1 in CAH-B patients responding to the IFN treatment were higher than those in non-responders or in which the anti-IFN activity was present. The anti-IFN activity may negatively influence the effect of the IFN therapy of CAH-B or CAH-C patients at early stages of the therapy. The appearance of the anti-IFN activity at the end of a long-term IFN therapy does not seem to influence the outcome of the therapy. sICAM-1 may be involved in the process of CAH-B reactivation and IFN-triggered cytotoxicity during the IFN therapy.
authors.affiliation: Institute of Preventive and Clinical Medicine, Bratislava, Slovak Republic.
authors.forename: D
authors.initials: D
authors.lastname: Stancek
authors.forename: N
authors.initials: N
authors.lastname: Fuchsberger
authors.forename: M
authors.initials: M
authors.lastname: Oltman
authors.forename: H
authors.initials: H
authors.lastname: Schmeisser
authors.forename: P
authors.initials: P
authors.lastname: Kontsek
authors.forename: E
authors.initials: E
authors.lastname: Jahnová
authors.forename: V
authors.initials: V
authors.lastname: Hajnická
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000032:analysis / Q000378:metabolism; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D006515:Hepatitis B virus / Q000187:drug effects; D019694:Hepatitis B, Chronic / Q000097:blood / Q000188:drug therapy / Q000276:immunology / Q000517:prevention & control; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy / Q000276:immunology; D006521:Hepatitis, Chronic / Q000188:drug therapy* / Q000473:pathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood* / Q000276:immunology / Q000378:metabolism; D007370:Interferon Type I / Q000494:pharmacology / Q000627:therapeutic use*; D016898:Interferon-alpha / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011863:Radioimmunoassay; D011994:Recombinant Proteins
chemical_list: D000998:Antiviral Agents; D007370:Interferon Type I; D016898:Interferon-alpha; D011994:Recombinant Proteins; D018799:Intercellular Adhesion Molecule-1; D000410:Alanine Transaminase