To address whether the Tat effect on the modulation of parasite infection requires the Tat-basic domain, we used a Tat mutant construct with the arginine (R) residues replaced by alanine (A) (Tat86-R(49–57)A) to evaluate whether both Tat constructs could activate the HIV-1-LTR reporter construct in THP-1 macrophages. The gene discussed is TAT; the disease is parasitic infectious disease.