[The human T-cell leukemia virus type I (HTLV-I) tax protein induces apoptosis]

Human T-cell leukemia virus type I (HTLV-I) is an etiological agent of adult T-cell leukemia. The Tax protein of HTLV-I may play a central role in cellular transformation. By serum deprivation, Tax-transformed Rat-1 cells undergo apoptotic cell death. These cells exhibit DNA fragmentation and chromatin condensation. Constitutive expression of bcl-2, blocked Tax-mediated apoptosis. Activation of fusion protein containing Tax and estrogen receptor, also led to the trans-activation and caused inhibition of proliferation and apoptosis. However Tax inhibited anti-Apo-1-induced apoptosis. Apoptosis appear to be the most important process of HTLV-I associated myelopathy (HAM). In spinal cords from autopsied patients with HAM/TSP, apoptosis of helper-inducer T lymphocytes was observed. HTLV-I carrier WKAH rats developed myeloneuropathy and apoptotic death of oligodendrocytes. The apoptosis was consistent with HTLV-I pX expression.