HIV-1 inhibits replication of HPC by inducing release of multiple mitotic inhibitory factors and expression of factors known to induce apoptosis. HIV-1–infected CD4⁺ T cells and HIV-1 tat released from infected cells induce release of IFN-γ^96,157 and TNF-α¹⁵⁸ from uninfected CD8⁺ T cells. HIV-1 and HIV-1 tat induce expression of IL-4 (which inhibits release of hematopoietic growth factors by other cells) and IL-4 receptors (IL-4R) thereby enhancing the “blunting” effect in lymphocytes159,160 and possibly stromal cells. IL-4 also induces stromal cells to release TGF-β¹⁶¹ and chemokine inhibitors.162 HIV-1 induction of fas ligand (FasL) in mononuclear phagocytes (M) and CD4⁺ cells results in apoptosis of uninfected CD4⁺ cells,163,164 but may also result in apoptosis of HPC which are known to express Fas under a variety of conditions. ^{57-59,165,166} Infection of macrophages also induces release of TNF-α,167,168TGF-β,169,170 and MIP1α.171 CD34⁺cells exposed to HIV-1 or HIV-1 gp120 release TGF-β,172 but while this has been called an “autocrine” response, it is not known whether the TGF-producing cells are actually progenitor cells, and is not, therefore, known to be a truly autocrine mechanism of HPC inhibition.