We analyzed IL-2 and IL-10 serum levels in 26 HIV-1-infected patients naive of antiretroviral treatment and in 34 patients receiving highly active antiretroviral therapy (HAART). All patients without treatment were asymptomatic. When they were stratified according to levels of CD4+ T cells, IL-2 levels were significantly increased in patients with > or =200 CD4+/microl and IL-10 levels were significantly increased in patients with <200 CD4+/microl compared to controls. A significant negative correlation was observed between IL10 levels and CD4+ T-cell counts. No correlation was observed between IL-2 and IL-10 levels and viral load due to the wide range of variability in the number of HIV copies/ml present in the different patients. However, IL-2 levels were higher in patients with high viral load than in patients with low viral load. In patients with HAART, IL-2 and IL-10 levels were similar to the control group and no differences were detected respecting CD4+ T cells counts and viral load. Our findings show that the modifications in IL-2 and IL-10 serum levels in HIV-1-infected patients naive of antiretroviral treatment are associated with the progression of immunological damage. Furthermore, they show a dysbalance of type-1/type-2 cytokines with an involvement of type-2 cytokines in later stages of HIV infection. Cytokine dysregulation can be reversed by HAART in the context of immune restoration and viral suppression.
Superoxide (O2−) production by polymorphonuclear neutrophils (PMN) was assessed in 17 subjects with asymptomatic infection (AI), 16 patients with acquired immunodeficiency syndrome (AIDS), and 12 healthy normal subjects. The effect of patients' serum on the oxidative activity of normal and patients' PMN was also investigated. The O2− production, nonstimulated and stimulated with zymosan particles in the presence of normal serum, was similar to that of normal controls in both groups of patients. The serum from 11 out of the 17 AI subjects (65%) induced an increase in the stimulated O2− production in normal and patients' PMN, while the serum from 8 out of the 16 AIDS patients (50%) induced a diminution. These effects did not appear to be related to complement C3 and circulating immune complex levels, but suggest that PMN of HIV‐seropositive patients do not present an intrinsic dysfunction and that the impact of serum factor(s) affects the normal oxidative activity of these cells depending on the stage of infection.
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