We do not yet know the mechanisms by which FoxP3 renders activated T-cells more susceptible to infection; however, two possibilities can be considered: (1) FoxP3 may be overcoming innate resistance factor(s) that accumulate in activated T-cells that block HIV infection, or (2) FoxP3 expression may be inducing critical host factors that are required for efficient completion of the HIV life cycle in primary T-cells. Here, FOXP3 is linked to HIV infectious disease.