Human T-cell lymphotrophic virus type I (HTLV-I) is a causative agent of adult T-cell leukemia (ATL). The viral transcriptional activator Tax encoded by the HTLV-I genome is thought to play critical roles in the activation of nuclear factor (${kappa}B;(NF-{kappa}B)$ as well as in the transformation of human T lymphocytes and the induction of tumor and leukemia. In this report, we suggest that RelA subunit of ${kappa}B$ might play an important role in Tax-induced p53 inactivation. Using antisense oligonucleotides, the ability of Tax inhibiting p53 transactivation was blocked by RelA, but not p50 or c-rel, antisense oligonucleotides in C81 HTLV-1-transfected cell line. The inability of p50 or c-rel antisense oligonucleotides in blocking the Tax-mediated inhibition of p53 function was not due lack of activity, since NF-${kappa}B$ activation was specifically blocked by these oligonucleotides. Also, we demonstrate by using co-immunoprecipitation assays that p53 interacts with RelA in HTLV-I transformed cells and their binding became stronger by the overexpression of Tax in 293T cells. These results suggest the possibility that the physical interaction between p53 and RelA correlates with Tax-induced p53 inhibition.