HTLV-1是在约5%的感染个体中引起ATL和其它炎性疾病如HAM/TSP和HU的致癌病毒。还已知HTLV-1感染的细胞保持无病,永生,潜伏状态贯穿约95%的感染者的一生。我们认为,载体中无病感染细胞的稳定维持是HTLV-1在人类生命周期中进化过程中获得的内在特征。我们推测病毒的发病机理由病毒蛋白的协调功能决定。特别是,雷克斯的监管,病毒复制率的导体,预计与病毒程序密切相关,在早期活跃的病毒复制,然后在HTLV-1感染的T细胞中稳定的潜伏期。HTLV-1和HIV-1属于逆转录病毒科,具有相同的向性,例如,人CD4+T细胞。这些病毒在病毒基因组结构和复制周期的分子机制方面显示出显著的相似性。然而,HTLV-1和HIV-1感染的T细胞表现出不同的表型,特别是在病毒体生产的水平。我们推测HTLV-1Rex及其对应的HIV-1Rev的活性如何受到调节可能与各自感染的T细胞的特性密切相关。在这次审查中,我们比较了HTLV-1和HIV-1的各种病理方面。特别是,我们调查了HTLV-1Rex或HIV-1Rev是否存在病毒编码的“调节阀”,以探讨其在受感染T细胞中病毒颗粒产生调节中的重要性.最后,根据我们最近对Rex的新功能方面的研究,我们确认Rex是病毒复制和病毒发病机理的关键导体。由于Rex的活性与病毒复制率密切相关,我们假设Rex活性的“调节阀”可能已经被选择性地进化以实现早期病毒颗粒产生和随后的长,在HTLV-1感染细胞中稳定的深潜伏期。
HTLV-1 is an oncovirus causing ATL and other inflammatory diseases such as HAM/TSP and HU in about 5% of infected individuals. It is also known that HTLV-1-infected cells maintain a disease-free, immortalized, latent state throughout the lifetimes of about 95% of infected individuals. We believe that the stable maintenance of disease-free infected cells in the carrier is an intrinsic characteristic of HTLV-1 that has been acquired during its evolution in the human life cycle. We speculate that the pathogenesis of the virus is ruled by the orchestrated functions of viral proteins. In particular, the regulation of Rex, the conductor of viral replication rate, is expected to be closely related to the viral program in the early active viral replication followed by the stable latency in HTLV-1 infected T cells. HTLV-1 and HIV-1 belong to the family Retroviridae and share the same tropism, e.g., human CD4+ T cells. These viruses show significant similarities in the viral genomic structure and the molecular mechanism of the replication cycle. However, HTLV-1 and HIV-1 infected T cells show different phenotypes, especially in the level of virion production. We speculate that how the activity of HTLV-1 Rex and its counterpart HIV-1 Rev are regulated may be closely related to the properties of respective infected T cells. In this review, we compare various pathological aspects of HTLV-1 and HIV-1. In particular, we investigated the presence or absence of a virally encoded \"regulatory valve\" for HTLV-1 Rex or HIV-1 Rev to explore its importance in the regulation of viral particle production in infected T cells. Finally, wereaffirm Rex as the key conductor for viral replication and viral pathogenesis based on our recent study on the novel functional aspects of Rex. Since the activity of Rex is closely related to the viral replication rate, we hypothesize that the \"regulatory valve\" on the Rex activity may have been selectively evolved to achieve the \"scenario\" with early viral particle production and the subsequent long, stable deep latency in HTLV-1 infected cells.