Genes of the major histocompatibility complex class II influence the outcome of hepatitis C virus infection

被引:200
作者
Alric, L
Fort, M
Izopet, J
Vinel, JP
Charlet, JP
Selves, J
Puel, J
Pascal, JP
Duffaut, M
Abbal, M
机构
[1] HOP PURPAN, SERV MED INTERNE, TOULOUSE, FRANCE
[2] HOP PURPAN, VIROL LAB, TOULOUSE, FRANCE
[3] HOP PURPAN, SERV HEPATOGASTROENTEROL, TOULOUSE, FRANCE
[4] HOP PURPAN, SERV ANATOMOPATHOL, TOULOUSE, FRANCE
[5] LAB SIGNALISAT & DIFFERENCIAT MACROPHAGES, INSERM, UNITE CJF9107, TOULOUSE, FRANCE
[6] HOP RANGUEIL, IMMUNOL LAB, TOULOUSE, FRANCE
[7] HOP HOTEL DIEU, SERV EPIDEMIOL, TOULOUSE, FRANCE
关键词
D O I
10.1053/gast.1997.v113.pm9352872
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: The host's immune response may influence the course of hepatitis C virus (HCV) infection. The aim of this study was to investigate the distribution of HLA class II alleles in white subjects who spontaneously recovered from HCV infection compared with that in patients with persistent infection. Methods: HLA-DRB1 and -DQB1 typing were performed in 103 consecutive patients with persistent HCV infection (HCV antibody positive, HCV RNA positive) and in 25 subjects with transient HCV infection (HCV antibody positive, persistently negative HCV RNA), Results: No significant differences between subjects with transient or persistent infection were observed for age, sex, source of infection, or HCV serotype. The frequency of DQB1*0301 and DRB1*1101 alleles was higher in patients with transient infection than in those with persistent infection (84% vs. 30.8%, 40% vs. 9.8%; P < 0.01 and P < 0.02, respectively [Bonferroni correction]), DRB1 and DQB1 alleles did not influence viral load as an independent factor. Mean Knodell's scores were lower in patients with DQB1*0301 allele (6.12 +/- 0.4) than in those negative for DQB1*0301 (7.37 +/- 0.3; P < 0.05). Conclusions: Our results suggest that host-rather than virus-related factors are probably involved in the spontaneous clearance of HCV.
引用
收藏
页码:1675 / 1681
页数:7
相关论文
共 38 条
[1]
HLA AND HEPATITIS-B INFECTION [J].
ALMARRI, A ;
BATCHELOR, JR .
LANCET, 1994, 344 (8931) :1194-1195
[2]
BEDOSSA P, 1994, HEPATOLOGY, V20, P15
[3]
USE OF NS-4 PEPTIDES TO IDENTIFY TYPE-SPECIFIC ANTIBODY TO HEPATITIS-C VIRUS GENOTYPE-1, GENOTYPE-2, GENOTYPE-3, GENOTYPE-4, GENOTYPE-5 AND GENOTYPE-6 [J].
BHATTACHERJEE, V ;
PRESCOTT, LE ;
PIKE, I ;
RODGERS, B ;
BELL, H ;
ELZAYADI, AR ;
KEW, MC ;
CONRADIE, J ;
LIN, CK ;
MARSDEN, H ;
SAEED, AA ;
PARKER, D ;
YAP, PL ;
SIMMONDS, P .
JOURNAL OF GENERAL VIROLOGY, 1995, 76 :1737-1748
[4]
BIGNON JD, 1995, HLA MED, P14
[5]
LYMPHOCYTE-T RESPONSE TO HEPATITIS-C VIRUS IN DIFFERENT CLINICAL COURSES OF INFECTION [J].
BOTARELLI, P ;
BRUNETTO, MR ;
MINUTELLO, MA ;
CALVO, P ;
UNUTMAZ, D ;
WEINER, AJ ;
CHOO, QL ;
SHUSTER, JR ;
KUO, G ;
BONINO, F ;
HOUGHTON, M ;
ABRIGNANI, S .
GASTROENTEROLOGY, 1993, 104 (02) :580-587
[6]
ISOLATION OF A CDNA CLONE DERIVED FROM A BLOOD-BORNE NON-A, NON-B VIRAL-HEPATITIS GENOME [J].
CHOO, QL ;
KUO, G ;
WEINER, AJ ;
OVERBY, LR ;
BRADLEY, DW ;
HOUGHTON, M .
SCIENCE, 1989, 244 (4902) :359-362
[7]
HLA class II genes in chronic hepatitis C virus-infection and associated immunological disorders [J].
Congia, M ;
Clemente, MG ;
Dessi, C ;
Cucca, F ;
Mazzoleni, AP ;
Frau, F ;
Lampis, R ;
Cao, A ;
Lai, ME ;
DeVirgiliis, S .
HEPATOLOGY, 1996, 24 (06) :1338-1341
[8]
Cramp M. E., 1996, Hepatology, V24, p151A
[9]
IMMUNOLOGICAL FEATURES AND HLA ASSOCIATIONS IN CHRONIC VIRAL-HEPATITIS [J].
CZAJA, AJ ;
CARPENTER, HA ;
SANTRACH, PJ ;
MOORE, SB .
GASTROENTEROLOGY, 1995, 108 (01) :157-164
[10]
SIGNIFICANCE OF HUMAN-LEUKOCYTE ANTIGENS DR3 AND DR4 IN CHRONIC VIRAL-HEPATITIS [J].
CZAJA, AJ ;
CARPENTER, HA ;
SANTRACH, PJ ;
MOORE, SB .
DIGESTIVE DISEASES AND SCIENCES, 1995, 40 (10) :2098-2106