Exposure to human immunodeficiency virus (HIV)-1 does not inevitably result in infection and resistance to HIV-1 infection is observed in different categories of at-risk individuals. In this study, the role of beta-chemokines and alpha-chemokine in providing resistance to HIV-1 infection was evaluated in a group of 25 HIV-exposed but uninfected (EU) partners of HIV-1-infected individuals. We studied the levels of regulated on activation, normal T expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta , and stromal cell-derived factor (SDF)-1alpha in culture supernatants of peripheral blood mononuclear cells (PBMCs) after stimulation with HIV gag p24 antigen and phytohemagglutinin (PHA). Higher gag-specific beta-chemokine responses were seen in EU individuals and HIV-positive controls when compared with healthy controls (HC). No significant difference was observed in PHA-specific beta-chemokine production between these three groups. Moreover, a spontaneous production of all the three beta-chemokines by unstimulated PBMCs was observed in EU individuals and HIV-positive controls. No significant difference was observed in alpha-chemokine (SDF-1) levels between the three groups after p24 and PHA stimulation. We conclude that in our cohort of EU individuals, beta-chemokines-mediated resistance against HIV might be present. Since beta-chemokines are produced mainly by activated T cells, our results suggest that enhanced chemokine production might be due to exposure to HIV in these individuals.
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Suresh et al. (2007) studied this question.