Abstract
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL). The minus strand of HTLV-1 provirus encodes a bZIP protein donated as HTLV-1 bZIP factor (HBZ). Among the HTLV-1 regulatory and accessory genes, the tax and HBZ genes were thought to play critical roles in oncogenesis. However, HBZ is the only gene that remains intact and is consistently expressed in all ATL cases, while the tax gene is frequently inactivated by epigenetic modifications or deletion of the 5’LTR. HBZ gene promotes the proliferation of ATL cells through its mRNA form. Moreover, HBZ induces T-cell lymphoma and systemic inflammation in vivo. HBZ fulfills its functions mainly through regulating HTLV-1 5’LTR transcription and modulating a variety of cellular signaling pathways which are related with cell growth, immune response, and T-cell differentiation. Taken together, the multiple functions of HBZ render its predominant function in leukemogenesis of ATL.
Highlights
Human T-cell leukemia virus type 1 (HTLV-1) was the first retrovirus proven to be associated with human disease
The characteristic of HTLV-1 proviral genome is the presence of pX region between env and 3 long terminal repeat (LTR), and encoded several accessory genes, which include tax, rex, p12, p21, p30, p13, and HTLV-1 basic ZIP domain (bZIP) factor (HBZ; Gaudray et al, 2002; Nicot et al, 2005)
HBZ was first identified as an antisense viral protein that associated with cAMP-response element binding protein-2 (CREB-2) in HTLV-1infected cells (Gaudray et al, 2002)
Summary
Human T-cell leukemia virus type 1 (HTLV-1) was the first retrovirus proven to be associated with human disease. The characteristic of HTLV-1 proviral genome is the presence of pX region between env and 3 LTR, and encoded several accessory genes, which include tax, rex, p12, p21, p30, p13, and HTLV-1 bZIP factor (HBZ; Gaudray et al, 2002; Nicot et al, 2005). HBZ was first identified as an antisense viral protein that associated with cAMP-response element binding protein-2 (CREB-2) in HTLV-1infected cells (Gaudray et al, 2002). 5 LTR of HTLV-1 was frequently lost and methylated in ATL cases, while 3 LTR was not deleted and remained unmethylated (Matsuoka and Jeang, 2007) It may be one of the reasons why HBZ is consistently expressed in all ATL cells. HBZ distributed in the nucleus to heterochromatin, while it is not associated with heterochromatin (Hivin et al, 2005)
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