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pubmed-article:1688521pubmed:abstractTextAlthough changes in function of monocytes from AIDS patients have previously been reported, the functional deficits that could occur in monocytes from asymptomatic HIV-seropositive individuals has not been extensively investigated. The goal of this study was to evaluate the oxidative burst response and cell surface marker expression of monocytes from this group. Both the oxidative burst, as measured by 2',7'-dichlorofluorescin diacetate oxidation, and cell surface markers were evaluated on CD14+ (Leu-M3) monocytes by two-color flow cytometry. A significantly lower oxidative burst capacity was observed in asymptomatic, seropositives after phorbol myristate acetate and calcium ionophore stimulation when compared to seronegative controls. However, differences in oxidative burst between the two groups were not observed after stimulation with heat-aggregated IgG. The oxidative burst of monocytes from seropositive HIV antigen+ or antigen- subjects was not significantly different. The most significant difference in monocyte surface markers between seropositive and seronegative controls was a decrease in the proportion of complement receptor 3+ (CD11b+) cells while slightly decreased numbers of CD13+ and CD33+ monocytes were observed. The decreased expression of CD11b+ cells in seropositives was found entirely within the seropositive, HIV antigen+ group. Similarly, when monocytes from seropositive HIV antigen+ and antigen- were compared, significantly lower numbers of CD4+ and HLA-DR+ cells were noted. These results indicate that significant changes in monocyte function and surface markers occur early during the course of HIV infection and are associated with the expression of serum HIV antigen.lld:pubmed
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pubmed-article:1688521pubmed:pagination184-91lld:pubmed
pubmed-article:1688521pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1688521pubmed:articleTitleDecreased oxidative burst activity of monocytes from asymptomatic HIV-infected individuals.lld:pubmed
pubmed-article:1688521pubmed:affiliationDepartment of Immunology/Microbiology, Rush-Presbyterian-St. Lukes Medical Center, Chicago, Illinois 60612.lld:pubmed
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pubmed-article:1688521pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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