Giam Chou-Zen, Jeang Kuan-Teh
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd., Bethesda, MD 20814, USA.
Front Biosci. 2007 Jan 1;12:1496-507. doi: 10.2741/2163.
Human T-lymphotropic virus type I (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATL) and HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 viral transactivator/oncoprotein, Tax, activates viral transcription and usurps regulatory mechanisms that are critical for cell growth and division to facilitate viral replication. The effects that Tax exerts on cells include potent NF-k B activation, cell cycle perturbation and cell transformation. How Tax influences ATL development is incompletely understood at present. While Tax-expression is needed at the early stages of cellular transformation, at later times most ATL cells do not express tax; therefore, genetic and epigenetic changes in HTLV-1-infected cells are believed to play an important role in the etiology of ATL. This review attempts to integrate recent literature on the biological activities of Tax and the properties of HTLV-1 transformed T-cells and ATL cells, and speculate on what cellular changes may collaborate with Tax to effect cell transformation and ATL development.
人类嗜T淋巴细胞病毒I型（HTLV-1）是成人T细胞白血病/淋巴瘤（ATL）和HTLV-1相关脊髓病/热带痉挛性截瘫（HAM/TSP）的病原体。HTLV-1病毒反式激活因子/癌蛋白Tax可激活病毒转录，并篡夺对细胞生长和分裂至关重要的调节机制，以促进病毒复制。Tax对细胞产生的影响包括强力激活NF-κB、扰乱细胞周期和细胞转化。目前，Tax如何影响ATL的发展尚未完全明确。虽然在细胞转化的早期阶段需要Tax表达，但在后期大多数ATL细胞并不表达tax；因此，HTLV-1感染细胞中的遗传和表观遗传变化被认为在ATL的病因学中起重要作用。本综述试图整合近期关于Tax生物学活性以及HTLV-1转化T细胞和ATL细胞特性的文献，并推测哪些细胞变化可能与Tax协同作用以实现细胞转化和ATL发展。
