Circulating immune complexes (ICs) were isolated by affinity chromatography and sucrose density gradient fractionation during acute and chronic hepatitis C virus (HCV) infection. Immunochemical and biomolecular studies showed that they basically consist of the virus component, IgG with specific anti-HCV activity and IgM bearing 17.109 epitope (IgM 17.109), an antigenic determinant common to rheumatoid factors (RFs) with WA cross-idiotype (XId). An antigen-specific IC assay was used to demonstrate IgG anti-HCV/IgM 17.109 ICs (IgG-IgM ICs) in five out of the five patients with acute and in 8 out of the 10 patients with chronic hepatitis C who mounted an IgG anti-HCV immune response. They were not detected in patients with no IgG anti-HCV response. IgG-IgM ICs appeared in step with IgG anti-HCV seroconversion and remained detectable for a long period irrespective of clinical outcome, in that they were demonstrated over a 4-year follow-up of patients with chronic hepatitis C. Their presence was unrelated to the severity and progression of liver histology. Despite similar serum levels of IgM 17.109 XId, antigen-specific IgG-IgM ICs were not found in acute and chronic hepatitis B or in acute hepatitis A. Thus, these ICs appear to be uniquely associated with HCV infection, supporting the view that IgM 17.109 XId derive from an antigen-driven response strictly related to the involved antigen. Even although they have no apparent effects on the progression of HCV-related liver disease, their presence may help to explain the immunological abnormalities and extrahepatic disorders observed in HCV infection.
IMMUNOCHEMICAL AND BIOMOLECULAR STUDIES OF CIRCULATING IMMUNE COMPLEXES ISOLATED FROM PATIENTS WITH ACUTE AND CHRONIC HEPATITIS C VIRUS INFECTION
SANSONNO, Domenico Ettore;LAULETTA, GIANFRANCO;
1996-01-01
Abstract
Circulating immune complexes (ICs) were isolated by affinity chromatography and sucrose density gradient fractionation during acute and chronic hepatitis C virus (HCV) infection. Immunochemical and biomolecular studies showed that they basically consist of the virus component, IgG with specific anti-HCV activity and IgM bearing 17.109 epitope (IgM 17.109), an antigenic determinant common to rheumatoid factors (RFs) with WA cross-idiotype (XId). An antigen-specific IC assay was used to demonstrate IgG anti-HCV/IgM 17.109 ICs (IgG-IgM ICs) in five out of the five patients with acute and in 8 out of the 10 patients with chronic hepatitis C who mounted an IgG anti-HCV immune response. They were not detected in patients with no IgG anti-HCV response. IgG-IgM ICs appeared in step with IgG anti-HCV seroconversion and remained detectable for a long period irrespective of clinical outcome, in that they were demonstrated over a 4-year follow-up of patients with chronic hepatitis C. Their presence was unrelated to the severity and progression of liver histology. Despite similar serum levels of IgM 17.109 XId, antigen-specific IgG-IgM ICs were not found in acute and chronic hepatitis B or in acute hepatitis A. Thus, these ICs appear to be uniquely associated with HCV infection, supporting the view that IgM 17.109 XId derive from an antigen-driven response strictly related to the involved antigen. Even although they have no apparent effects on the progression of HCV-related liver disease, their presence may help to explain the immunological abnormalities and extrahepatic disorders observed in HCV infection.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
