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IL‐2 and IL‐10 serum levels in HIV‐1‐infected patients with or without active antiretroviral therapy
Author(s) -
ORSILLES MIGUEL ÁNGEL,
PIERI ELSA,
COOKE PAULA,
CAULA CINTHYA
Publication year - 2006
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2006.apm_108.x
Subject(s) - viral load , immunology , asymptomatic , medicine , immune system , cytokine , context (archaeology) , interleukin 10 , lentivirus , antiretroviral therapy , immunopathology , viral disease , human immunodeficiency virus (hiv) , biology , paleontology
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 ≥200 CD4+/μl and IL‐10 levels were significantly increased in patients with <200 CD4+/μl 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.