Highly active antiretroviral therapy (HAART) is able to cause lipid metabolism and glucose homeostasis alterations, which are associated to the redistribution of body fat. Alterations in lipid and carbohydrate metabolism contribute to the development of a highly atherogenic profile, which together with altered fibrinolysis markers and increased presence of proinflammatory cytokines in blood (especially tumor necrosis factor alpha) that comes associated to the success of HAART can cause the development of accelerated atherosclerosis. Docosahexaenoic acid (DHA) is a polyunsaturated fatty acid that has demonstrated its ability to reduce triglyceride levels; modify cholesterol fractions and increase the size of LDL particles thereby configuring less atherogenic plasma profile. Additionally, administration of DHA has shown antiinflammatory and hypotensive activity, which contributes to reduce the risk of cardiovascular complications in these patients. At a molecular level, DHA acts as a stimulator of the nuclear receptor PPAR-gamma, which has been described to induce an increase in adipocyte differentiation. Furthermore, the anti-inflammatory effects induced by DHA, can decrease the elevated levels of TNF-alpha, which has been implicated in the pathogenesis of body fat redistribution in HIV infected patients undergoing HAART. Therefore, the hypothesis of this project is that DHA will be able to produce lipid-lowering, anti-inflammatory, hypotensive and profibrinolytic effects, which all together should improve atherogenic profile of patients with HIV-1 infection receiving HAART. In addition, their proprieties as PPAR agonist can improve the redistribution of body fat present in many of these patients. The study of the activity of DHA on dendritic cells and monocytes should indicate the absence of immunosuppressive effect of DHA in the context of HIV-1 infection.