[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.
Yamada
T
T
Radiation Biology Center Kyoto University.
D000818:Animals; D017209:Apoptosis; D002472:Cell Transformation, Viral; D016356:Gene Products, tax / Q000502:physiology; D006801:Humans; D015493:Paraparesis, Tropical Spastic / Q000209:etiology; D051381:Rats; D013601:T-Lymphocytes
D016356:Gene Products, tax