Prevalence of GBV-C/HGV-RNA, virus genotypes, and anti-E2 antibodies in autoimmune hepatitis.
OBJECTIVE
We investigated the prevalence of hepatitis G-RNA (GBV-C/HGV-RNA), a recently cloned new flavivirus, and of antibodies to the envelope 2 antigen (anti-E2), a marker of past infection, in patients with autoimmune hepatitis, and compared it with the prevalence in patients with chronic viral hepatitis and healthy control individuals.


METHODS
Sera of 63 patients with autoimmune hepatitis were studied for the presence of GBV-C/HGV-RNA by reverse-transcription polymerase chain reaction and for anti-E2 by enzyme-linked immunosorbent assay. GBV-C/HGV genotypes were determined by genome sequencing.


RESULTS
Patients with autoimmune hepatitis had a similar high prevalence of GBV-C/HGV-RNA and anti-E2 antibodies as patients with chronic viral hepatitis B or C. GBV-C/HGV-RNA was found significantly more often in patients with autoimmune hepatitis (11%, p = 0.045), hepatitis B (16%, p = 0.004), or hepatitis C (21%, p = 0.001) than in healthy controls (2%). The prevalence of anti-E2 antibodies in patients with autoimmune hepatitis was not different from healthy controls (17% vs 13%, NS). The various subtypes of autoimmune hepatitis had similar prevalence rates of GBV-C/HGV-RNA as patients with liver-kidney microsomal antibody-positive hepatitis C. All of our anti-E2+ (GBV-C/HGV-RNA-) patients were positive for anti-smooth-muscle antibody, whereas only 29% of GBV-C/HGV-RNA+ (anti-E2-) patients were positive (p = 0.025). All seven of the GBV-C/HGV-RNA+ patients with autoimmune hepatitis had genotype 2a, which is also the most prevalent genotype in our region.


CONCLUSIONS
The prevalence of GBV-C/HGV-RNA is significantly increased in patients with autoimmune hepatitis, compared with healthy controls, and is similar to the increased prevalence seen in chronic hepatitis B or C patients. Anti-E2 positivity was associated with antibodies against smooth-muscle antigen in all cases. All GBV-C/HGV+ autoimmune hepatitis patients were infected with genotype 2a.
Tribl
B
B
Universitätsklinik für Innere Medizin IV, Klinische Abteilung Gastroenterologie und Hepatologie, University of Vienna, Austria.
Schöniger-Hekele
M
M
Petermann
D
D
Bakos
S
S
Penner
E
E
Müller
C
C
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000906:Antibodies / Q000032:analysis; D000914:Antibodies, Viral / Q000032:analysis; D000956:Antigens, Viral / Q000032:analysis*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D018067:Flaviviridae / Q000235:genetics* / Q000276:immunology; D005838:Genotype; D019694:Hepatitis B, Chronic / Q000276:immunology / Q000821:virology; D019698:Hepatitis C, Chronic / Q000276:immunology / Q000821:virology; D019693:Hepatitis, Autoimmune / Q000276:immunology / Q000821:virology*; D006801:Humans; D007668:Kidney / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis*; D008861:Microsomes / Q000276:immunology; D008862:Microsomes, Liver / Q000276:immunology; D008875:Middle Aged; D009130:Muscle, Smooth / Q000276:immunology; D016133:Polymerase Chain Reaction; D015995:Prevalence; D012367:RNA, Viral / Q000235:genetics*; D017423:Sequence Analysis, RNA; D014759:Viral Envelope Proteins / Q000032:analysis*
D000906:Antibodies; D000914:Antibodies, Viral; D000956:Antigens, Viral; D008562:Membrane Glycoproteins; D012367:RNA, Viral; D014759:Viral Envelope Proteins; C107619:glycoprotein E2, GB virus C