HLA class II favors clearance of HCV infection and progression of the chronic liver damage

Citation
A. Mangia et al., HLA class II favors clearance of HCV infection and progression of the chronic liver damage, J HEPATOL, 30(6), 1999, pp. 984-989
Citations number
24
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
JOURNAL OF HEPATOLOGY
ISSN journal
01688278 → ACNP
Volume
30
Issue
6
Year of publication
1999
Pages
984 - 989
Database
ISI
SICI code
0168-8278(199906)30:6<984:HCIFCO>2.0.ZU;2-D
Abstract
Background/Aims: This study was aimed to determine whether host-dependent g enetic factors modulate the outcome of HCV infection. Methods HLA class II DRB and DQB typing was performed in 184 infected patie nts and 200 healthy volunteers. Among the patients, 149 subjects had persis tent HCV viremia (Group I) and 35 subjects underwent spontaneous viral clea rance (Group 2), Group 1 included cirrhotic patients with transfusion-acqui red infections (n=79), asymptomatic MCV carriers (n= 42), and patients with chronic hepatitis C responsive to interferon therapy (n=28), Results: Spontaneous viral clearance was associated with HLA DRB1*1104 (pc= 0.054, OR=4.51, 95% C,I, 2.02 10.1) and HLA DQB1*0301 (pc=0.0039, OR=4.52, 95% C,I, 2.15-9.51), In Group 1 the haplotype DRB1*1104/DQB1*0301 was less frequent (4.8%) than in Group 2 (18.3%) (pc=0.009, OR= 7.38, 95% C,I, 2.58- 21.59), At the HLA levels cirhotic patients were not different from asympto matic HCV carriers and patients with interferon-induced viral clearance, In cirrhotic patients infected with genotype Ib, the DQB1*0502 allele was mor e frequently found in those with rapidly progressive liver damage (OR=8.15, 95% C,I, 1.49-4.44),but the corrected p-value was not significant (pc=0.09 ), Conclusions: The HLA haplotype DRB1*1104/DQB1*0301 appears Co contribute to the spontaneous clearance of HCV infection. The predominance of the DQB1*0 502 allele in cirrhotic patients with arapidly progressive disease possibly reflects an influence of this allele on the progression of the HCV-related liver disease.