The interaction of human T-cell lymphotropic virus I (HTLV-I) tax gene with host cell factors plays an important role in the maintenance of the transformed state. There have been numerous reports that have demonstrated the role of tax in transactivating several cytokines. In this study, we show that upon mitogen stimulation, macrophage inflammatory protein-1 beta (MIP-1 beta) is expressed and secreted in tax-transfected Jurkat cells. Furthermore, expression of CC-chemokine receptor-5 (CCR5) mRNA in these cells suggests an autocrine role for MIP-1 beta in HTLV-I-infected T-cells. These results, coupled with our earlier observations, demonstrate the influence that extracellular Tax protein might have on modulating host chemokines for proliferation and transformation of uninfected cells.