title: Increased concentrations of soluble tumor necrosis factor receptor 75 but not of soluble intercellular adhesion molecule-1 are associated with the decline of CD4+ lymphocytes in HIV infection.
abstract: Immune activation seems to be involved in the pathogenesis of human immunodeficiency virus (HIV) infection. The immune activation markers neopterin and beta 2-microglobulin can predict the future rate of the decrease in CD4+ T cells. In a longitudinal study, we assessed whether the decline in the CD4+ T-cell count is associated with increased concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble tumor necrosis factor receptor 75 (sTNFR 75), compared to increased concentrations of beta 2-microglobulin and urinary neopterin. Forty-seven individuals representing all stages of HIV infection were followed-up for a mean of 12.7 months (range, 8 to 16 months). The percentage of the change of the CD4+ T-cell count from study entry to study end ranged from -97 to +98%; the median was -33%. Concentrations of urinary neopterin, sTNFR 75, and beta 2-microglobulin correlated with the percentage of the change of the CD4+ T-cell count from study entry to study end (r = -0.45, confidence interval (CI) -0.65 to -0.19; r = -0.42, 95% CI -0.63 to -0.15; and r = -0.416, 95% CI -0.62 to -0.15), but those of sICAM-1 did not. This difference was found despite significant correlations between sICAM-1 and sTNFR 75 and beta 2-microglobulin. Levels of sICAM-1 obtained at study entry correlated with levels of sICAM-1 obtained at study end (r = 0.46, 95% CI 0.17 to 0.68). In a multivariate linear regression analysis, urinary neopterin and sTNFR 75 were jointly significant for the percentage of the change of the CD4+ T-cell count. These results suggest that sTNFR 75 is a useful marker to estimate disease progression in HIV infection, whereas sICAM-1 does not seem to provide any information related to the decline of the CD4+ T-cell count.
authors.affiliation: Department of Dermatology and Venereology, University of Innsbruck, Austria.
authors.forename: R
authors.initials: R
authors.lastname: Zangerle
authors.forename: D
authors.initials: D
authors.lastname: Fuchs
authors.forename: M
authors.initials: M
authors.lastname: Sarcletti
authors.forename: H
authors.initials: H
authors.lastname: Gallati
authors.forename: G
authors.initials: G
authors.lastname: Reibnegger
authors.forename: H
authors.initials: H
authors.lastname: Wachter
authors.forename: M P
authors.initials: MP
authors.lastname: Dierich
authors.forename: J
authors.initials: J
authors.lastname: Möst
mesh_terms: D000328:Adult; D015703:Antigens, CD; D001708:Biopterins / Q000031:analogs & derivatives / Q000652:urine; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D015815:Cell Adhesion Molecules / Q000097:blood* / Q000737:chemistry; D005260:Female; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D007958:Leukocyte Count; D008297:Male; D019798:Neopterin; D018124:Receptors, Tumor Necrosis Factor / Q000737:chemistry / Q000378:metabolism*; D047889:Receptors, Tumor Necrosis Factor, Type II; D012995:Solubility; D001613:beta 2-Microglobulin / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D001613:beta 2-Microglobulin; D018799:Intercellular Adhesion Molecule-1; D001708:Biopterins; D019798:Neopterin