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
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.