CCR5A32 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C

作     者：Ankur Goyal PV Suneetha GT Kumar Deepak K Shukla Naveen Arora Shiv K Sarin 

作者机构：Department of Gastroenterology G.B.Pant HospitalNew DelhiInstitute of Genomic and Integrative Biology(Formerly CBT)Mall RoadDelhiDr.Ambedkar Center for Biomedical ResearchUniversity of DelhiIndia Department of Gastroenterology G.B.Pant HospitalNew DelhiIndia Division of Non-communicable Disease Indian Council of Medical ResearchAnsari NagarNew DelhiIndia Institute of Genomic and Integrative Biology (Formerly CBT)Mall RoadDelhiIndia 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2006年第12卷第29期

页      面：4721-4726页

核心收录：

学科分类：1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 100401[医学-流行病与卫生统计学] 10[医学] 

基　　金：National Task Force Project from the Indian Council of Medical Research supported by Council of Scientific and Industrial Research (CSIR)  New Delhi to Ankur Goyal  a Senior Research Fellow 

主　　题：β-chemokine receptor 32 bp deletion CCchemokine ligand Human leukocyte antigen Histologicalactivity index 

摘      要：AIM： To study whether CCR5△32 mutation was associated with viral infection and severity of liver disease. METHODS： Two hundred and fifty two histologically proven, chronic HCV patients （mean age： 41±14 years; M/F： 164/88） were genotyped. PCR based genotyping of 32 bp deletion at the CCR5 locus was done. Fourhundred and eight matched healthy controls were studied to assess susceptibility to HCV infection. To assess correlation of immune gene polymorphism with severity of HCV related liver disease, patients with chronic HCV infection were divided into those with a fibrosis score of ≤ 2 （mild） or 〉 2 （severe） and histological activity index （HAI） of ≤ 5 or 〉 5. For correlation between CCR5△32 mutations and response to therapy, 129 patients who completed therapy were evaluated. RESULTS： The majority （89.4%） of the patients were infected with genotype 3. The frequency of homozygous CCR5△32 mutants was comparable to HCV patients as compared to the healthy controls （0.7% vs 0%, P = 0.1）. Further more, the frequency of CCR5△32 mutation was comparable in patients with mild or severe liver disease.（P = NS）. There was also no association observed with response to therapy and CCR5△32 mutation. CONCLUSION： CCR5△32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection.