Human Leukocyte Antigen Class I and II Alleles and Response to Interferon‐α Treatment, in Taiwanese Patients with Chronic Hepatitis C Virus Infection | Zendy

MingLung Yu | Zendy; ChiaYen Dai | Zendy; ShinnCherng Chen | Zendy; ChaoChin Chiu | Zendy; LiPo Lee | Zendy; ZuYau Lin | Zendy; MingYuh Hsieh | Zendy; LiangYen Wang | Zendy; WanLong Chuang | Zendy; WenYu Chang | Zendy

Open Access

Human Leukocyte Antigen Class I and II Alleles and Response to Interferon‐α Treatment, in Taiwanese Patients with Chronic Hepatitis C Virus Infection

Author(s) -

MingLung Yu,

ChiaYen Dai,

ShinnCherng Chen,

ChaoChin Chiu,

LiPo Lee,

ZuYau Lin,

MingYuh Hsieh,

LiangYen Wang,

WanLong Chuang,

WenYu Chang

Publication year - 2003

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/375554

Subject(s) - immunology , immunogenetics , hepatitis c virus , interferon , allele , haplotype , genotype , linkage disequilibrium , virus , biology , alpha interferon , hepacivirus , human leukocyte antigen , cirrhosis , virology , antigen , medicine , gene , genetics

To investigate the influence of immunogenetics on response to interferon (IFN)-alpha treatment, human leukocyte antigen alleles were characterized in 100 unrelated Taiwanese patients with chronic hepatitis C virus (HCV) infection. A11, B51, Cw15, and DRB1*15 were positively correlated with sustained response, whereas A24 was inversely associated with response to IFN-alpha, after adjustment for cirrhosis, pretreatment virus load, and viral genotype. Homozygote-genotype analysis showed that A24 and DQB1*05 probably had gene-dosage effect on sustained response. DRB1*15 was in strong linkage disequilibrium with DQB1*05 and DQB1*06, but only haplotype DRB1*15-DQB1*05 was associated with response to IFN-alpha. Haplotype A11-DRB1*15 was strongly associated with sustained response. This suggests a role for a complex host-immunogenetics interplay in the response to IFN-alpha, in patients with chronic HCV infection.

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