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The Human T-cell leukemia virus type 1 basic leucine zipper protein (HBZ) is a critical regulatory protein encoded by the antisense strand of the HTLV-1 provirus (Matsuoka & Green, Retrovirology 2009). It plays a pivotal role in the maintenance of viral latency and the oncogenic transformation of T-cells, being constitutively expressed in Adult T-cell leukemia/lymphoma (ATL) cells even when the sense-strand protein Tax is silenced (Satou et al., PNAS 2006). HBZ functions as a transcription factor that modulates host cell signaling pathways by interacting with various cellular partners, including CREB, JunD, and p300/CBP, thereby promoting cell survival and proliferation while evading the host immune response (Mitobe et al., Cancer Science 2015). Beyond its role in ATL, HBZ is also implicated in the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) through its influence on chronic inflammatory processes (Saito et al., Frontiers in Microbiology 2013). Because of its indispensable role in the viral life cycle and disease progression, HBZ is a primary target for novel therapeutic approaches, such as antisense oligonucleotides and peptide-based vaccines, aimed at treating HTLV-1-related malignancies and inflammatory disorders.
Inhibition of HBZ mRNA or protein function to suppress T-cell proliferation and induce apoptosis in HTLV-1 infected cells.
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