These data suggest thatthe frequency of HIV-specific CD8+T cells is maintained during the chronic phaseof infection, their ability to function is compromised and is not a reflection of ART.While the addition of IL-2, anti-CD40L and allogeneic cells led to partial increasein the ability of the tetramer+ cells to synthesize IFN-γ, the addition of IL-4, IL-12,anti-CD28 or a cocktail of anti-TGF-β, TNF-α and IL-10 failed to augment the IFN-γ response. The gene discussed is CD28; the disease is infection.