title: Host-pathogen interactions in the development of metabolic disturbances and atherosclerosis in HIV infection: the role of CCL2 genetic variants.
abstract: BACKGROUND
  Circulating CCL2 concentration has been implicated in promoting atherosclerosis in patients infected with HIV. We evaluated whether CCL2 gene variants are associated with metabolic disturbances and plasma CCL2 levels in HIV-infected patients.
  
  
  RESULTS
  CCL2 genotypes and estimated haplotypes, plasma CCL2 levels and indicators of metabolic status in HIV-infected patients were compared with a representative group of the general population. We also performed a carotid/femoral artery ultrasonography to detect sub-clinical atherosclerosis in these patients. Six haplotypes were estimated in more than the 5% of individuals, and accounted for more than 98% of the population. In HIV-infected patients, carriers of H1, H2 and H5 haplotypes had higher CCL2 concentration than carriers of H3, H4 and H6 haplotypes. However, only carriers of H1 and H5 haplotypes presented higher insulin resistance as well as higher proportion of patients affected with sub-clinical. Conversely, carriers of H2 haplotype, which also showed high plasma CCL2 concentration, were associated with less deleterious metabolic disturbances.
  
  
  CONCLUSIONS
  Our data are consistent with the hypothesis that the genetic background of the host is involved in CCL2 production and that this chemokine is implicated in promoting metabolic disturbances and sub-clinical atherosclerosis in HIV-infected patients.
authors.affiliation: Servei de Medicina Interna, Hospital Universitari de Sant Joan, IISPV, Universitat Rovira i Virgili, Reus, Spain. quinavir@gmail.com
authors.forename: Carlos
authors.initials: C
authors.lastname: Alonso-Villaverde
authors.forename: Gerard
authors.initials: G
authors.lastname: Aragonès
authors.forename: Raúl
authors.initials: R
authors.lastname: Beltrán-Debón
authors.forename: Laura
authors.initials: L
authors.lastname: Fernández-Sender
authors.forename: Anna
authors.initials: A
authors.lastname: Rull
authors.forename: Fernando
authors.initials: F
authors.lastname: Rodríguez-Sanabria
authors.forename: Judit
authors.initials: J
authors.lastname: Marsillach
authors.forename: Pedro
authors.initials: P
authors.lastname: Pardo-Reche
authors.forename: Jordi
authors.initials: J
authors.lastname: Camps
authors.forename: Jorge
authors.initials: J
authors.lastname: Joven
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000150:complications* / Q000378:metabolism*; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood / Q000235:genetics*; D005260:Female; D014644:Genetic Variation; D015658:HIV Infections / Q000097:blood / Q000150:complications* / Q000378:metabolism*; D006239:Haplotypes / Q000235:genetics; D054884:Host-Pathogen Interactions / Q000235:genetics*; D006801:Humans; D015810:Linkage Disequilibrium / Q000235:genetics; D008297:Male; D008954:Models, Biological
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2