HBZ

HBZ, short for HTLV-1 basic leucine zipper factor, is a regulatory protein associated with human T-lymphotropic virus type 1 (HTLV-1). It is produced from the antisense strand of the integrated viral provirus and exists as both an RNA transcript and a protein product. The HBZ transcript can be spliced, and the encoded protein contains a basic region–leucine zipper (bZIP) domain that enables dimerization with host transcription factors and nuclear localization. HBZ expression is a characteristic feature of HTLV-1–infected cells and is detectable in many cases of adult T-cell leukemia/lymphoma (ATLL), even when other viral genes are silenced.

Functionally, HBZ modulates host gene expression and viral transcription. The HBZ protein interacts with members of the AP-1 family, such as Jun proteins, and can antagonize Tax-mediated transactivation of HTLV-1, contributing to viral persistence. In addition to the protein, HBZ RNA has regulatory roles that influence cell proliferation, differentiation, and immune evasion. Overall, HBZ promotes T-cell proliferation and survival and is implicated in the development and maintenance of ATLL.

Clinically, HBZ serves as a molecular marker of HTLV-1 infection and is central to understanding ATLL pathogenesis. Because Tax is often targeted by the host immune response, HBZ helps sustain oncogenic signaling in malignant cells. Research into HBZ continues, including efforts to develop therapies that disrupt HBZ function or its interactions with host factors.