Satou Yorifumi
Laboratory of Virus Control, Institute for Virus Research, Kyoto University.
Uirusu. 2012 Jun;62(1):113-20. doi: 10.2222/jsv.62.113.
HTLV-1 is a retrovirus associated with human diseases, such as ATL or HAM/TSP. More than thirty years have passed since HTLV-1 was discovered, but the precise mechanism of HTLV-1 pathogenesis still remains elusive. HTLV-1 bZIP factor (HBZ) was reported ten years ago as a viral gene encoded in the minus strand of HTLV-1. We have elucidated that HBZ is constitutively detectable in all ATL cells examined whereas tax expression is frequently lost. Furthermore, we and other researchers have reported that HBZ expression contributes to the proliferation of infected cells. We have shown that HBZ has the potential to transform T cells in vivo by analyzing HBZ-transgenic mice. Further investigations will uncover a more detailed role of HBZ in HTLV-1 pathogenesis. This paradigm shift of HTLV-1 research should provide novel target in prevention or treatment of HTLV-1-related human diseases.
人类嗜T淋巴细胞病毒1型(HTLV-1)是一种与人类疾病相关的逆转录病毒,如成人T细胞白血病(ATL)或热带痉挛性截瘫(HAM/TSP)。自HTLV-1被发现以来,已经过去了三十多年,但HTLV-1发病机制的精确细节仍然不清楚。HTLV-1碱性亮氨酸拉链因子(HBZ)在十年前作为一个编码于HTLV-1负链的病毒基因被报道。我们已经阐明,在所有检测的ATL细胞中均能持续检测到HBZ,而tax表达常常缺失。此外,我们和其他研究人员报道,HBZ表达有助于受感染细胞的增殖。通过分析HBZ转基因小鼠,我们已经表明HBZ有在体内转化T细胞的潜力。进一步的研究将揭示HBZ在HTLV-1发病机制中更详细的作用。HTLV-1研究的这种范式转变应该会为预防或治疗HTLV-1相关人类疾病提供新的靶点。