Abstract
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.
