Given our previous observations that Tat (and TGF-β) augment surface CD91/LRP-1 on macrophages, on one hand, and that HIV-1 infection enhances Leishmania internalization in uninfected bystander MDMs, on the other, we set out to determine if virus infection promotes either TGF-β secretion or activation. The gene discussed is TGFB1; the disease is viral infectious disease.