title: Frequency of the HIV-protective CC chemokine receptor 5-Delta32/Delta32 genotype is increased in hepatitis C.
abstract: OBJECTIVE
  A homozygous 32-base pair deletion in the CCR5 gene (CCR5-Delta32) protects against human immunodeficiency virus infection (HIV). However, the role of this mutation in other infections, such as hepatitis C virus (HCV) infection, has not been defined.
  
  
  METHODS
  We determined the frequency of the CCR5-Delta32 mutation by polymerase chain reaction in anti-HCV(+) (n = 153), anti-HIV(+) (n = 102), and anti-HCV(+)/HIV(+) (n = 130) white patients as well as in 102 healthy blood donors. Then, HIV and HCV loads, aminotransferases, and CD4 and CD8 cell counts were compared between the resulting subsets of CCR5-Delta32/wild-type heterozygotes, CCR5-Delta32, and wild-type homozygotes, respectively.
  
  
  RESULTS
  Twelve of 153 (7.8%) anti-HCV-seropositive patients and 1 of 102 (1.0%) healthy blood donors were CCR5-Delta32 homozygous, whereas CCR5-Delta32 homozygosity was absent in anti-HIV(+) and anti-HCV(+)/HIV(+) patients (P < 0.001). The frequency of the CCR5-Delta32 allele was higher in the anti-HCV(+) (16.0%, P < 0.05) and anti-HCV(+)/HIV(+) (12.7%, NS) patients than in healthy blood donors (8.3%) and anti-HIV(+) patients (9.3%), respectively. Anti-HCV(+) CCR5-Delta32 homozygotes occurred 3 times more frequently than expected from the Hardy-Weinberg equation (P < 0.0001) and had significantly higher HCV loads than wild-type patients (P = 0.045).
  
  
  CONCLUSIONS
  The increased prevalence of CCR5-Delta32 homozygosity associated with increased viral loads in patients with chronic hepatitis C suggests that the CCR5-Delta32 mutation may be an adverse host factor in hepatitis C.
authors.affiliation: Department of Internal Medicine I, University of Bonn, Bonn, Germany. Woitas@uni-bonn.de
authors.forename: Rainer P
authors.initials: RP
authors.lastname: Woitas
authors.forename: Golo
authors.initials: G
authors.lastname: Ahlenstiel
authors.forename: Agathe
authors.initials: A
authors.lastname: Iwan
authors.forename: Jürgen K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: Hans H
authors.initials: HH
authors.lastname: Brackmann
authors.forename: Bernd
authors.initials: B
authors.lastname: Kupfer
authors.forename: Bertfried
authors.initials: B
authors.lastname: Matz
authors.forename: Ruth
authors.initials: R
authors.lastname: Offergeld
authors.forename: Tilman
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: Ulrich
authors.initials: U
authors.lastname: Spengler
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000483:Alleles; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D015483:HIV Antibodies / Q000032:analysis; D015658:HIV Infections / Q000517:prevention & control*; D006526:Hepatitis C / Q000235:genetics* / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000032:analysis; D006720:Homozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D019713:Receptors, CCR5 / Q000235:genetics*; D012016:Reference Values; D019562:Viral Load
chemical_list: D015483:HIV Antibodies; D018937:Hepatitis C Antibodies; D019713:Receptors, CCR5