Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) ; A cross-sectional study was performed on HIV-1 infected individuals with or without antiretroviral treatment (ARV) in the AIDS Day Hospital, Botucatu Medical School, UNESP. Between August 2004 and October 2005, 73 HIV-1 infected individuals were divided into three groups: infected individuals with or without AIDS who had never received ARV (G(1) = 15); patients on HAART that had had plasma HIV-1 RNA viral load (VL) equal to or greater than 50 copies/mL (G(2) = 27); and patients on HAART with undetectable VL for at least the past six months (G(3) = 31). There was also an additional group that comprised blood donors without any sign of the disease and with negative HIV serum tests (G(4) = 20), which was the control group. Serum cytokine levels (values in pg/mL) were measured by enzyme-linked immunosorbent assay (ELISA) and specific mRNA expression by reverse transcription polymerase chain reaction (RT-PCR). Both techniques were performed on the four groups for TNF-alpha, IL-2, INF-gamma, IL-4 and IL-10. All patients were submitted to VL determination and CD4(+) and CD8(+) T lymphocyte counts. The analysis of the results revealed a significant comparison among groups for both methods and an association between the latter (>80% - r(2) > 0.80). There was only one exception, in control individuals for IL-2 by ELISA. The cytokine profiles, in both methods, for the three patient groups, were mature Th-0. The behaviors of IL-2 and INF-gamma required emphasis due to consequent expression of dominant Th profile. Both methods showed low IL-2 and high mean values of INF-gamma in the three groups. Several authors have recently drawn attention to the substantial apoptosis of infected and non-infected CD4(+) T cells, mainly during primary infection, persisting only in those with INF-gamma phenotype producer and not IL-2. HIV infected individuals submitted to HAART are expected to produce IL-2 in an attempt to present Th-1 profile, but in most cases this did not occur.