Enhances viral infectivity and persistence, and facilitates proliferation of HTLV-1-infected lymphocytes (PubMed:16424388). Mechanistically, inhibits Tax-mediated viral replication and NF-kappa-B activation (PubMed:18599479, PubMed:21552325). Plays a role in allowing infected T-cells to escape the cytotoxic T-lymphocyte response by maintaining low levels of viral protein production. Inhibits also host EP300 histone acetyltransferase (HAT) activity, reducing levels of acetylated histone H3 at 'Lys-18' (H3K18ac) in infected cells (PubMed:22434882). Contributes to the accumulation of chromosomal abnormalities by inhibiting double-stranded DNA breaks (DSB) repair through the NHEJ pathway (PubMed:29769340). Participates in the modulation of host immune response at multiple levels contributing to abnormal interferon signaling and viral pathogenesis (PubMed:28768861). Interacts with host ATF4; this interaction inhibits viral RNA transcriptional activation by preventing ATF4 binding to Tax-responsive elements. Interacts with host CREB1; this interaction inhibits host CREB1 transcriptional activity. Interacts with host JUN, JUNB and JUND (By similarity). Interacts with host EP300 and CREBBP; these interactions inhibit the association of the coactivators with the viral promoter (PubMed:18599479, PubMed:22434882). Interacts with host UBR5; this interaction regulates HBZ protein stability (PubMed:29441057). Interacts with XRCC5 and XRCC6 (PubMed:29769340). Interacts with IRF7 and IKBKE; this interaction modulates host interferon signaling (PubMed:28768861). Contains three nuclear localization signals NLS-1 and NLS-2, corresponding to two regions rich in basic amino acids, and NLS-3 corresponding to its DNA-binding domain. Ubiquitinated by host E3 ligase UBR5 leading to HBZ degradation. Expressed from antisense transcripts. While mRNA expression levels of HBZ-SI were similar to those of HBZ, HBZ-SI seems slightly more expressed at the protein level ex vivo. Belongs to the HTLV-1 HBZ protein family.