title: Lack of higher frequency of the chemokine receptor 5-delta32/delta32 genotype in hepatitis C.
abstract: OBJECTIVE
  An elevated frequency of the CCR5-Delta32 mutation in German patients with hepatitis C with viremia has been reported. The aim of the present study was to verify whether this mutation occurs in an Italian population with hepatitis C and whether it is an adverse host factor indicative of severity of liver disease and response to antiviral therapy.
  
  
  METHODS
  The authors amplified 189-bp (wild-type) and 157-bp (Delta32 deletion) fragments of the CCR5 gene by polymerase chain reaction in 130 patients with chronic hepatitis C. Comparisons were drawn with 110 blood donors and 135 patients with primary biliary cirrhosis.
  
  
  RESULTS
  Four (3.1%) patients with chronic hepatitis C and 1 blood donor (0.9%) were CCR5-Delta32 homozygous, whereas there was no CCR5-Delta32 homozygosity among primary biliary cirrhosis patients; the wild-type gene was present in a similar percentage in the 3 groups of patients without any significant difference (83.1% vs 90.4% vs 83.6%, respectively). Among the patients with chronic hepatitis C, no significant correlation was found between CCR5-Delta32 homozygosity and the following parameters: histologic grade/stage, hepatitis C virus genotype, viral load, serum aspartate aminotransferase, serum alanine aminotransferase, and serum gamma-glutamyltransferase. Ninety-five patients received a standard antiviral protocol with pegylated interferon (PEG Intron)+ribavirin; a sustained response was achieved in 59 patients (62.1%), and the remainder did not respond or experienced a relapse. Response to treatment was not influenced by CCR5-Delta32 deletion.
  
  
  CONCLUSIONS
  No greater frequency of CCR5-Delta32 homozygosity was seen in an Italian population of patients with chronic hepatitis C. This mutation does not seem to influence either the overall severity of liver disease or the response to viral therapy.
authors.affiliation: Department of Surgical and Gastroenterological Sciences, University of Padova, Italy.
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Tommasi
authors.forename: Paolo
authors.initials: P
authors.lastname: Fabris
authors.forename: Isabella
authors.initials: I
authors.lastname: Carderi
authors.forename: Anna
authors.initials: A
authors.lastname: Baragiotta
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Baldo
authors.forename: Carla
authors.initials: C
authors.lastname: Venturi
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Giordani
authors.forename: Giulia
authors.initials: G
authors.lastname: Tositti
authors.forename: Annarosa
authors.initials: A
authors.lastname: Floreani
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use; D016009:Chi-Square Distribution; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000235:genetics*; D006720:Homozygote; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D007558:Italy; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D019713:Receptors, CCR5 / Q000235:genetics*; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D019713:Receptors, CCR5; D007372:Interferons