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CCR△532 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C
引用本文:Goyal A,Suneetha PV,Kumar GT,Shukla DK,Arora N,Sarin SK. CCR△532 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C[J]. World journal of gastroenterology : WJG, 2006, 12(29): 4721-4726. DOI: 10.3748/wjg.v12.i29.4721
作者姓名:Goyal A  Suneetha PV  Kumar GT  Shukla DK  Arora N  Sarin SK
作者单位:[1]Department of Gastroenterology, G.B. Pant Hospital, New Delhi, Institute of Genomic and Integrative Biology, (Formerly CBT), Mall Road, Delhi, Dr. Ambedkar Center for Biomedical Research, University of Delhi, India [2]Department of Gastroenterology, G.B. Pant Hospital, New Delhi, India [3]Division of Non-communicable Disease, Indian Council of Medical Research, Ansari Nagar, New Delhi, India [4]Institute of Genomic and Integrative Biology, (Formerly CBT), Mall Road, Delhi, India
摘    要:

关 键 词:基因突变  磁化率  丙型病毒肝炎  肝疾病
收稿时间:2005-08-17

CCR5Delta32 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C
Goyal Ankur,Suneetha P V,Kumar G T,Shukla Deepak K,Arora Naveen,Sarin Shiv K. CCR5Delta32 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C[J]. World journal of gastroenterology : WJG, 2006, 12(29): 4721-4726. DOI: 10.3748/wjg.v12.i29.4721
Authors:Goyal Ankur  Suneetha P V  Kumar G T  Shukla Deepak K  Arora Naveen  Sarin Shiv K
Affiliation:Department of Gastroenterology, G.B. Pant Hospital, University of Delhi, New Delhi-110002 and Adjunct Professor, Molecular Medicine, Jawaharlal Lal Nehru University, New Delhi, India.
Abstract:AIM: To study whether CCR5Delta32 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. Four-hundred 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 CCR5Delta32 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 CCR5Delta32 mutants was comparable to HCV patients as compared to the healthy controls (0.7% vs 0%, P = 0.1). Further more, the frequency of CCR5Delta32 mutation was comparable in patients with mild or severe liver disease. (P = NS). There was also no association observed with response to therapy and CCR5Delta32 mutation. CONCLUSION: CCR5Delta32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection.
Keywords:β-chemokine receptor 32 bp deletion   CC chemokine ligand   Human leukocyte antigen   Histological activity index
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