title: Lack of effect of chemokine receptor CCR2b gene polymorphism (64I) on HIV-1 plasma RNA viral load and immune activation among HIV-1 seropositive female workers in Abidjan, Côte d'Ivoire.
abstract: The prevalence of the CCR2b-V64I mutation among human immunodeficiency virus (HIV)-seropositive and -seronegative female workers and the potential effect of heterozygosity of this mutation on HIV-1 plasma RNA viral load and markers of immune activation were assessed. CCR2b-V64I was detected by polymerase chain reaction, followed by restriction enzymes analysis; plasma viral load was measured by the Amplicor HIV-1 monitor assay and CD4(+) T-cell counts and markers of immune activation by standard three-color FACscan flow cytometry. Of the 260 female workers, 56 (21.5%) were heterozygous for CCR2b-V64I, and 8 (3%) were homozygous. Of the 99 HIV-seronegative female workers, 19 (19.2%) were heterozygous for the CCR2b-V64I mutation compared with 37 (23%) of the 161 HIV-seropositive FSW (P = 0.47). In a univariate analysis of viral load among HIV-seropositive FSW, no difference was noted between those heterozygous for or without the mutation; both groups had plasma viral loads of 5.0 log(10) copies/ml. After controlling for the effects of CD4(+) T-cell counts in a multivariate analysis, no significant difference was observed between the groups in viral load or in markers of immune activation. The data suggest that the presence of the CCR2b mutation has no effect on HIV-1 plasma viral load and markers of immune activation in our study population. The finding that the frequency of this mutation is similar in HIV-seropositive and -seronegative female workers suggests that its presence is not associated with increased risk of HIV infection.
authors.affiliation: Projet RETRO-CI, Abidjan, Côte d'Ivoire.
authors.forename: C A
authors.initials: CA
authors.lastname: Adjé
authors.forename: C E
authors.initials: CE
authors.lastname: Bilé
authors.forename: L
authors.initials: L
authors.lastname: Kestens
authors.forename: S
authors.initials: S
authors.lastname: Koblavi-Deme
authors.forename: P D
authors.initials: PD
authors.lastname: Ghys
authors.forename: C
authors.initials: C
authors.lastname: Maurice
authors.forename: M
authors.initials: M
authors.lastname: Kalou-Badirou
authors.forename: N
authors.initials: N
authors.lastname: Kabran
authors.forename: R E
authors.initials: RE
authors.lastname: Ekpini
authors.forename: T H
authors.initials: TH
authors.lastname: Roels
authors.forename: S Z
authors.initials: SZ
authors.lastname: Wiktor
authors.forename: J N
authors.initials: JN
authors.lastname: Nkengasong
mesh_terms: D000328:Adult; D018932:Chemokine CCL2 / Q000235:genetics*; D015331:Cohort Studies; D007560:Cote d'Ivoire; D005260:Female; D015658:HIV Infections / Q000235:genetics* / Q000276:immunology / Q000821:virology; D018023:HIV Seronegativity / Q000235:genetics / Q000276:immunology; D006679:HIV Seropositivity / Q000235:genetics* / Q000276:immunology / Q000821:virology; D015497:HIV-1; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D011110:Polymorphism, Genetic; D054390:Receptors, CCR2; D019707:Receptors, Chemokine / Q000235:genetics*; D015728:Receptors, HIV / Q000235:genetics*; D019562:Viral Load
chemical_list: C515334:CCR2 protein, human; D018932:Chemokine CCL2; D054390:Receptors, CCR2; D019707:Receptors, Chemokine; D015728:Receptors, HIV