title: Distribution and effects of polymorphic RANTES gene alleles in HIV/HCV coinfection -- a prospective cross-sectional study.
abstract: OBJECTIVE
  Chemokines and their receptors are crucial for immune responses in HCV and HIV infection. RANTES gene polymorphisms lead to altered gene expression and influence the natural course of HIV infection. Therefore, these mutations may also affect the course of HIV/HCV coinfection.
  
  
  METHODS
  We determined allele frequencies of RANTES-403 (G --> A), RANTES-28 (C --> G) and RANTES-IN1.1 (T --> C) polymorphisms using real-time PCR and hybridization probes in patients with HIV (n = 85), HCV (n = 112), HIV/HCV coinfection (n = 121), and 109 healthy controls. Furthermore, HIV and HCV loads as well as CD4(+) and CD8(+) cell counts were compared between different RANTES genotypes.
  
  
  RESULTS
  Frequencies of RANTES-403 A, RANTES-28 G and RANTES-IN1.1 C alleles were higher in HIV infected patients than in healthy controls (-403: 28.2% vs 15.1%, P = 0.002; -28: 5.4% vs 2.8%, not significant; IN1.1: 19.0% vs 11.0%, P = 0.038). In HIV/HCV coinfected patients, these RANTES alleles were less frequent than in patients with HIV infection alone (15.4% P = 0.002; 1.7%; P = 0.048; 12.0%; not significant). Frequencies of these alleles were not significantly different between HIV/HCV positive patients, HCV positive patients and healthy controls.
  
  
  CONCLUSIONS
  All three RANTES polymorphisms showed increased frequencies of the variant allele exclusively in patients with HIV monoinfection. The finding that the frequencies of these alleles remained unaltered in HIV/HCV coinfected patients suggests that HCV coinfection interferes with selection processes associated with these alleles in HIV infection.
authors.affiliation: Medizinische Klinik u Poliklinik 1, Universitatsklinikum Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany.
authors.forename: Golo
authors.initials: G
authors.lastname: Ahlenstiel
authors.forename: Agathe
authors.initials: A
authors.lastname: Iwan
authors.forename: Jacob
authors.initials: J
authors.lastname: Nattermann
authors.forename: Karin
authors.initials: K
authors.lastname: Bueren
authors.forename: Jurgen 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: Olfert
authors.initials: O
authors.lastname: Landt
authors.forename: Amnon
authors.initials: A
authors.lastname: Peled
authors.forename: Tilman
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: Ulrich
authors.initials: U
authors.lastname: Spengler
authors.forename: Rainer P
authors.initials: RP
authors.lastname: Woitas
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D018946:Chemokine CCL5 / Q000097:blood / Q000235:genetics*; D002648:Child; D003430:Cross-Sectional Studies; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications / Q000235:genetics*; D006239:Haplotypes; D006526:Hepatitis C / Q000150:complications / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D019713:Receptors, CCR5 / Q000097:blood
chemical_list: D018946:Chemokine CCL5; D019713:Receptors, CCR5