Characteristic expression of HTLV-1 basic zipper factor (HBZ) transcripts in HTLV-1 provirus-positive cells

To investigate the role of HBZ-SI in HTLV-1 provirus-positive cells, the HBZ-SI and Tax mRNA loads in samples with a mixture of infected and non-infected cells were measured and then adjusted by dividing by the HTLV-I proviral load. We show here that the HBZ-SI mRNA level is 4-fold higher than non-spliced HBZ and is expressed by almost all cells harboring HTLV-1 provirus with variable intensity. The proviral-adjusted HBZ-SI and Tax quantification revealed a characteristic imbalanced expression feature of high HBZ and low Tax expression levels in primary ATL cells or high HBZ and very high Tax levels in HTLV-1-related cell lines (cell lines) compared with a standard expression profile of low HBZ and low Tax in infected cells. Interestingly, according to the mutual Tax and HBZ expression status, HTLV-1-related cell lines were subcategorized into two groups, an ATL cell type with high HBZ and low Tax levels and another type with high Tax and either high or low HBZ, which was closely related to its cell origin.This is the first comprehensive study to evaluate the mutual expression profile of HBZ and Tax in provirus-positive cells, revealing that there are quantitative and relative characteristic features among infected cells, primary ATL cells, and cell lines.Adult T-cell leukemia (ATL) is a unique T-cell malignancy derived from T-cells infected with a retrovirus of human T-cell leukemia virus type-1 (HTLV-1) [1-3]. ATL is clinically and hematologically characterized to develop step by step through smoldering, chronic, and acute stages after a long latency of HTLV-1 infection, revealing that ATL is a good experimental model of multi-step carcinogenesis.Although it is a fact that HTLV-1 reaches an oncogenic event and causes ATL, the oncogenic mechanism of HTLV-1 is not fully understood. The HTLV-1 genome, in addition to the structural and enzymatic proteins gag, pol, and env, encodes the regulatory and accessory proteins tax, rex, p12I, p13II, and p30II [4,5]. Among thes