Yoshida M
Banyu Tsukuba Research Institute, Tsukuba, Ibaraki 300-2611, Japan.
Annu Rev Immunol. 2001;19:475-96. doi: 10.1146/annurev.immunol.19.1.475.
The human T cell leukemia virus-1 (HTLV-1) is a retrovirus that causes adult T cell leukemia (ATL) and neurological disorder, the tropical spastic paraparesis (HAM/TSP). The pathogenesis apparently results from the pleiotropic function of Tax protein, which is a key regulator of viral replication. Tax exerts (a) trans-activation and -repression of transcription of different sets of cellular genes through binding to groups of transcription factors and coactivators, (b) dysregulation of cell cycle through binding to inhibitors of CDK4/6, and (c) inhibition of some tumor suppressor proteins. These effects on a wide variety of cellular targets seem to cooperate in promoting cell proliferation. This is an effective viral strategy to amplify its proviral genome through replication of infected cells; ultimately it results in cell transformation and leukemogenesis.
人类T细胞白血病病毒1型（HTLV-1）是一种逆转录病毒，可导致成人T细胞白血病（ATL）和神经系统疾病——热带痉挛性截瘫（HAM/TSP）。其发病机制显然源于Tax蛋白的多效性功能，Tax蛋白是病毒复制的关键调节因子。Tax通过与多组转录因子和共激活因子结合，对不同细胞基因集的转录发挥（a）反式激活和抑制作用，（b）通过与细胞周期蛋白依赖性激酶4/6（CDK4/6）抑制剂结合来失调细胞周期，以及（c）抑制某些肿瘤抑制蛋白。这些对多种细胞靶点的作用似乎协同促进细胞增殖。这是一种通过感染细胞的复制来扩增其前病毒基因组的有效病毒策略；最终导致细胞转化和白血病发生。
