title: [Do polymorphisms of the SDF1 and CCR2b genes modify the course of hepatitis C or HIV/HCV co-infection?].
abstract: OBJECTIVE
  Complementary to the CCR5-Delta32 mutation polymorphisms in the genes of CCR2b (CCR2b-V64 I) and stromal derived factor (SDF)-1 (SDF-1 3'A) affect the course of the human immunodeficiency virus (HIV) infection. While the CCR5-Delta32 mutation is also increased in chronic hepatitis C virus (HCV) infection it is unclear, whether the CCR2b-V64 I and the SDF-1 3'A polymorphisms also are associated with chronic HCV infection.
  
  
  METHODS
  We analyzed the frequencies of the CCR2b-V64I and SDF1 - 3'A mutation in patients with HIV/HCV coinfection (n = 130), HIV infection (n = 105), HCV infection (n = 153) and 112 healthy blood donors. We stratified each group into homozygous mutations, heterozygous mutations and homozygous wild types, respectively. The resulting subsets were compared with respect to HIV and HCV loads, CD4 and CD8 cell counts.
  
  
  RESULTS
  The mutant SDF1 - 3'A allele was found at 20.3 % frequency in patients with HCV infection and at 20.4 % frequency in patients with HIV/HCV coinfection, respectively. It was present in 27.1 % of the patients with HIV infection and 27.9 % of the healthy controls (not significant). The number of SDF-1 3) A homozygous patients was highest in patients with HIV/HCV coinfection and significantly different compared to the Hardy-Weinberg equilibrium (p = 0.010, chi (2) = 9.15). However, CD4- and CD8-cell counts or viral loads were not affected by this mutation. The frequency of the CCR2b-V64 I allele was similar in all patient groups. However, CCR2b-V64 I heterozygous patients showed HIV loads that were threefold lower than in CCR2b wildtype patients (22.9 x 103 vs. 6.4 x 103 copies/ml, not significant). Furthermore, hepatitis C viral loads were reduced roughly by 30 %.
  
  
  CONCLUSIONS
  These results suggest that the SDF1 - 3'A and CCR2b-V64I mutations do not affect the course of HCV and HIV/HCV infection in the same manner as does the CCR5-Delta32 mutation.
authors.affiliation: Medizinische Klinik und Poliklinik I, Hugstetter, Freiburg, Germany. Woitas@uni-bonn.de
authors.forename: R P
authors.initials: RP
authors.lastname: Woitas
authors.forename: G
authors.initials: G
authors.lastname: Ahlenstiel
authors.forename: A
authors.initials: A
authors.lastname: Iwan
authors.forename: J K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: H H
authors.initials: HH
authors.lastname: Brackmann
authors.forename: B
authors.initials: B
authors.lastname: Kupfer
authors.forename: B
authors.initials: B
authors.lastname: Matz
authors.forename: R
authors.initials: R
authors.lastname: Offergeld
authors.forename: T
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: U
authors.initials: U
authors.lastname: Spengler
mesh_terms: D000293:Adolescent; D000328:Adult; D016516:CD4-CD8 Ratio; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D015658:HIV Infections / Q000150:complications / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications / Q000235:genetics*; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000235:genetics*; D019562:Viral Load
chemical_list: C515334:CCR2 protein, human; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D054390:Receptors, CCR2; D019707:Receptors, Chemokine