CC chemokine receptor 5 cell-surface expression in relation to CC chemokine receptor 5 genotype and the clinical course of HIV-1 infection

Citation
Ad. Husman et al., CC chemokine receptor 5 cell-surface expression in relation to CC chemokine receptor 5 genotype and the clinical course of HIV-1 infection, J IMMUNOL, 163(8), 1999, pp. 4597-4603
Citations number
33
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
163
Issue
8
Year of publication
1999
Pages
4597 - 4603
Database
ISI
SICI code
0022-1767(19991015)163:8<4597:CCR5CE>2.0.ZU;2-X
Abstract
CCR5 cell-surface expression was studied in relation to CCR5 genotype and c linical course of HIV-1 infection. HIV-1 infected CCR5(+/+) individuals had higher percentages of CCR5-expressing CD4(+) T cells as compared with HIV- l-infected CCR5(32/+). individuals. For both genotypic groups, the percenta ges of CCR5-expressing cells were higher than for the uninfected counterpar ts CCR5(+/+), HIV+ 28% and HIV- 15% (p < 0.0001); CCR5(32/+), HIVS. 21% and HIV- 10% (p = 0.001), respectively). In HIV-l-infected individuals, high p ercentages of CCRS-expressing cells were associated with low CD4(+) T cell numbers (p = 0.001), high, viral RNA load in serum (p = 0.016), and low T c ell function (p = 0.053). As compared with nonprogressors with similar CD4( +) T cell numbers, individuals who did progress to AIDS had a higher percen tage of CCR5-expressing CD4(+) T cells (32% vs 21% (p = 0.001). Longitudina l analysis of CCRSf/' individuals revealed slight, although not statistical ly significant, increases in CCRS-expressing CD4(+) T cells and CD4(+) T ce ll subsets characterized by the expression of CD45 isoforms, during the cou rse of HIV-1 infection. Preseroconversion, the percentage of CCR5-expressin g CD4(+) T cells was higher in individuals who subsequently developed AIDS (28%) than in those who did not show disease progression within a similar t ime frame (20%;p = 0.059), Our data indicate that CCR5 expression increases with progression of disease, possibly as a consequence of continuous immun e activation associated with HIV-1 infection, In turn, CCR5 expression may influence the clinical course of infection.