Abstract
In a previous work we have evaluated some immunologic and haematologic parameters of HIV‐1 positive subjects co‐infected with HHV‐8. A worsening of these values were generally described in these patients as compared with those HIV‐1 positive, but negative for HHV‐8. Now we have studied the influence of HHV‐8 co‐infection of HIV‐1 positive subjects on the production of some cytokines to make clear the question of its role in the immuno‐deregulation of the above‐mentioned subjects. In particular we have analysed serum levels of IL‐4 and IL‐10, Th2 type T cells cytokines, IFN‐γ, an indirect marker of Th1 cells activation and IL‐18, a cytokine produced by monocytic‐macrophagic cells, which is able to induce IFN‐γ production and Th1 T lymphocytes activation. No significant differences were found as regards the IFN‐γ serum levels (92.1 ± 24.3 pg ml^−1^ in the case of HIV‐1 positive/HHV‐8 negative subjects and 96.0 ± 17.4 pg ml^−1^ in those HIV‐1 positive/HHV‐8 positive). In healthy subjects the mean level of this cytokine was 17.6 ± 5.2 pg ml^−1^ (significant difference with both the former values at p < 0.001). Moreover IL‐4 and IL‐10, which were undetectable in healthy individuals, showed the following values in HIV‐1positive/HHV‐8 negative subjects: 31.9 ± 2.7 pg ml^−1^ and 119.8 ± 85.1 pg ml^−1^ respectively and in HIV‐1 positive/HHV‐8 positive subjects: 30.4 ± 4.8 pg ml^−1^ and 69.4 ± 65.3 pg ml^−1^ (not significant differences). In contrast IL‐18 reached a mean level of 1001.2 ± 360.5 pg ml^−1^ in HIV‐1 positive/HHV‐8 negative subjects, but showed a significant reduction in HIV‐1 positive/HHV‐8 positive subjects (737.6 ± 284.3 pg ml^−1^→p < 0.05) and presented very low levels in healthy individuals (21.3 ± 30.3 pg ml^−1^). Moreover a significant correlation (−0.984→p < 0.001) was noticed between IL‐18 reduction in HIV‐1 positive subjects co‐infected with HHV‐8 and the degree of positivity of HHV‐8. These data suggest that HHV‐8 co‐infection has no influence on the switch Th1→ Th2 in HIV‐1 positive subjects, but is able to reduce IL‐18 production, useful for Th1 subset restoration. Copyright © 2002 John Wiley & Sons, Ltd.