title: The stromal derived factor-1 mutated allele (SDF1-3'A) is associated with a lower incidence of atherosclerosis in HIV-infected patients.
abstract: BACKGROUND
  HIV-infected patients have higher rates of subclinical atherosclerosis. The chemokine stromal derived factor 1 (SDF-1) is the natural ligand for the CXCR4 HIV co-receptor, is highly expressed in atherosclerotic plaques, and the plasma concentration is lower in individuals homozygous for the mutant allele (SDF1-3'A). We tested the influence of SDF1-3'A on atherosclerosis in HIV-infected patients.
  
  
  METHODS
  We performed carotid ultrasonography and determined the SDF1-3'A DNA polymorphism in 183 HIV-infected patients. Classical cardiovascular risk factors and antiretroviral therapy were also recorded. From these patients, we selected a group of 134 patients taking protease inhibitor-based antiretroviral therapy and in whom the lipid profile over an 18-month follow-up was collated.
  
  
  RESULTS
  We found atherosclerosis in 113 (61.7%) and a lower number of patients with the SDF-1 mutated allele in the group with carotid atherosclerosis compared to those without (41.6% versus 57.1%; P = 0.04). Using a logistic regression analysis, age and dyslipidaemia were significantly associated with atherosclerosis but the SDF1-3'A allele exerted a protective effect on the development of atherosclerosis (odds ratio, 0.45; 95% confidence interval, 0.14-1.02; P = 0.05). Further, we observed that, in the selected group of patients there were lower plasma low-density lipoprotein cholesterol concentrations [mean +/- SEM, 2.06 +/- 0.34 mmol/l] throughout follow up in those patients without carotid lesions and who also carried the mutated SDF1-3'A allele (P = 0.04).
  
  
  CONCLUSIONS
  The SDF1-3'A allele is associated with a lower presence of subclinical carotid atherosclerosis in an HIV-infected population.
authors.affiliation: Institut de Recerca en Ciències de la Salut, Hospital Universitari de Sant Joan, Reus, Spain. bcoll@grupsagessa.com
authors.forename: Blai
authors.initials: B
authors.lastname: Coll
authors.forename: Carlos
authors.initials: C
authors.lastname: Alonso-Villaverde
authors.forename: Sandra
authors.initials: S
authors.lastname: Parra
authors.forename: Manuel
authors.initials: M
authors.lastname: Montero
authors.forename: Monica
authors.initials: M
authors.lastname: Tous
authors.forename: Jorge
authors.initials: J
authors.lastname: Joven
authors.forename: Lluis
authors.initials: L
authors.lastname: Masana
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D002340:Carotid Artery Diseases / Q000235:genetics* / Q000473:pathology / Q000821:virology; D016022:Case-Control Studies; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000235:genetics*; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000150:complications / Q000235:genetics* / Q000473:pathology; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors; D017539:Tunica Intima / Q000473:pathology
chemical_list: C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D008055:Lipids