AIM: To study whether CCR5A32 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 CCR5A32 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 CCR5A32 mutants was comparable to HCV patients as compared to the healthy controls (0.7% vs 0%, P = 0.1). Further more, the frequency of CCR5A32 mutation was comparable in patients with mild or severe liver disease. (P=NS). There was also no association observed with response to therapy and CCR5A32 mutation. CONCLUSION: CCR5A32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection. 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 For 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 CCR5A32 mutations and response to therapy, 129 patients who completed The majority (89.4%) of the patients were infected with genotype 3. The frequency of homozygous CCR5A32 mutants was comparable to HCV patients as compared to the healthy controls (0.7% vs 0%, P = 0.1). Fu rther more, the frequency of CCR5A32 mutation was comparable in patients with mild or severe liver disease. (P = NS). There was also no association observed with response to therapy and CCR5A32 mutation. CONCLUSION: CCR5A32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection.