title: CCR5Delta32 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  CCR5Delta32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection.
authors.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.
authors.forename: Ankur
authors.initials: A
authors.lastname: Goyal
authors.forename: P V
authors.initials: PV
authors.lastname: Suneetha
authors.forename: G T
authors.initials: GT
authors.lastname: Kumar
authors.forename: Deepak K
authors.initials: DK
authors.lastname: Shukla
authors.forename: Naveen
authors.initials: N
authors.lastname: Arora
authors.forename: Shiv K
authors.initials: SK
authors.lastname: Sarin
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000483:Alleles; D000998:Antiviral Agents / Q000627:therapeutic use*; D016022:Case-Control Studies; D018450:Disease Progression; D004359:Drug Therapy, Combination; D005260:Female; D020022:Genetic Predisposition to Disease; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D011092:Polyethylene Glycols; D019713:Receptors, CCR5 / Q000235:genetics*; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use*; D012720:Severity of Illness Index
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D019713:Receptors, CCR5; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D000410:Alanine Transaminase; C417083:peginterferon alfa-2b