AUTOIMMUNE MECHANISMS IN CHRONIC HEPATITIS-B AND DELTA-VIRUS INFECTIONS

Citation
Bm. Mcfarlane et al., AUTOIMMUNE MECHANISMS IN CHRONIC HEPATITIS-B AND DELTA-VIRUS INFECTIONS, European journal of gastroenterology & hepatology, 7(7), 1995, pp. 615-621
Citations number
NO
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
0954691X
Volume
7
Issue
7
Year of publication
1995
Pages
615 - 621
Database
ISI
SICI code
0954-691X(1995)7:7<615:AMICHA>2.0.ZU;2-R
Abstract
Objective: To investigate the possibility that hepatitis delta virus i nfection may be responsible for, or enhance, the autoreactivity seen i n patients chronically infected with hepatitis B virus. Design: Sera f rom 68 patients with chronic hepatitis B infection, 27 of whom had con comitant 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) anti bodies against the putative autoantigen, GOR, which have been describe d in patients with HCV infection and (3) antibodies against a hepatocy te-specific autoantigen, the asialoglycoprotein receptor (ASGP-R). Met hods: Anti-GOR antibodies were detected using an enzyme-linked immunos orbent assay against a synthetic COR peptide, non-organ-specific autoa ntibodies using standard indirect immunofluorescence and anti-ASGP-R a ntibodies using a radioimmunoassay. Results: Liver-specific autoreacti vity, manifested by circulating anti-ASGP-R antibodies, was found in 4 1 (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-g astric parietal cell and anti-liver-kidney microsomal type 1) were fou nd (mostly at low titres) in only 15 (22.1%) patients and did not corr elate with either HDV infection or with histological severity. Basal c ell layer antibodies and type 3 liver-kidney microsomal antibodies wer e not seen in any patient. Antibodies against GOR were found in only f ive (7.4%) patients, all of whom showed evidence of exposure to HCV. C onclusion: The findings suggest that HBV-induced liver-specific autore actions might contribute to periportal liver damage in patients with c hronic hepatitis B infection, but do not support the notion that the d elta virus can induce an autoimmune response or that HCV coinfection s uppresses autoreactivity in this situation.