title: Autoimmune mechanisms in chronic hepatitis B and delta virus infections.
abstract: OBJECTIVE
  To investigate the possibility that hepatitis delta virus infection may be responsible for, or enhance, the autoreactivity seen in patients chronically infected with hepatitis B virus.
  
  
  METHODS
  Sera from 68 patients with chronic hepatitis B infection, 27 of whom had concomitant delta virus (HDV) infection and 19 of whom were infected with hepatitis C virus (HCV), were screened for (1) the non-organ-specific autoantibodies usually associated with autoimmune hepatitis, (2) antibodies against the putative autoantigen, GOR, which have been described in patients with HCV infection and (3) antibodies against a hepatocyte-specific autoantigen, the asialoglycoprotein receptor (ASGP-R).
  
  
  METHODS
  Anti-GOR antibodies were detected using an enzyme-linked immunosorbent assay against a synthetic GOR peptide, non-organ-specific autoantibodies using standard indirect immunofluorescence and anti-ASGP-R antibodies using a radioimmunoassay.
  
  
  RESULTS
  Liver-specific autoreactivity, manifested by circulating anti-ASGP-R antibodies, was found in 41 (60.3%) patients and correlated independently with the histological severity of liver damage but not with HDV infection. In contrast, non-organ-specific autoantibodies (antinuclear, anti-smooth muscle, anti-gastric parietal cell and anti-liver-kidney microsomal type 1) were found (mostly at low titres) in only 15 (22.1%) patients and did not correlate with either HDV infection or with histological severity. Basal cell layer antibodies and type 3 liver-kidney microsomal antibodies were not seen in any patient. Antibodies against GOR were found in only five (7.4%) patients, all of whom showed evidence of exposure to HCV.
  
  
  CONCLUSIONS
  The findings suggest that HBV-induced liver-specific autoreactions might contribute to periportal liver damage in patients with chronic hepatitis B infection, but do not support the notion that the delta virus can induce an autoimmune response or that HCV coinfection suppresses autoreactivity in this situation.
authors.affiliation: Institute of Liver Studies, King's College Hospital and School of Medicine and Dentistry, London, UK.
authors.forename: B M
authors.initials: BM
authors.lastname: McFarlane
authors.forename: C B
authors.initials: CB
authors.lastname: Bridger
authors.forename: H M
authors.initials: HM
authors.lastname: Smith
authors.forename: K A
authors.initials: KA
authors.lastname: Antonov
authors.forename: N
authors.initials: N
authors.lastname: Naoumov
authors.forename: R
authors.initials: R
authors.lastname: Williams
authors.forename: I G
authors.initials: IG
authors.lastname: McFarlane
mesh_terms: D000328:Adult; D037263:Asialoglycoprotein Receptor; D001212:Asialoglycoproteins / Q000276:immunology; D001323:Autoantibodies / Q000032:analysis*; D015551:Autoimmunity / Q000276:immunology*; D016022:Case-Control Studies; D005260:Female; D006509:Hepatitis B / Q000276:immunology*; D006526:Hepatitis C / Q000276:immunology; D003699:Hepatitis D / Q000276:immunology*; D006521:Hepatitis, Chronic / Q000276:immunology*; D006801:Humans; D008099:Liver / Q000276:immunology; D008297:Male; D011956:Receptors, Cell Surface / Q000276:immunology
chemical_list: D037263:Asialoglycoprotein Receptor; D001212:Asialoglycoproteins; D001323:Autoantibodies; D011956:Receptors, Cell Surface