Abstract
Adult T-cell leukemia (ATL) is a leukemia derived from mature CD4+ T cells and induced by human T-cell leukemia virus type 1 (HTLV-1) infection. Previous studies have revealed many possible molecular and cellular mechanisms of HTLV-1-induced leukemogenesis, but it still remains unknown how HTLV-1 transforms peripheral CD4 T cells in infected individuals. Given the fact that only 2–5% of infected individuals develop ATL, HTLV-1 infection alone is not sufficient for the transformation of infected cells. Host genetic and epigenetic abnormalities and host immunological status should be considered in attempting to understand the mechanism of the oncogenesis of ATL. Nonetheless, it is obvious that HTLV-1 infection dramatically increases the risk of leukemia generation from peripheral CD4 T-cells, in which the incidence of leukemia is quite low. Furthermore, the evidence that all ATL cases retain the HTLV-1 provirus, especially the 3′ region, indicates that HTLV-1-encoded genes play a critical role in leukemogenesis. Since increasing evidence indicates that the HTLV-1 bZIP factor (HBZ) gene plays a significant role in the pathogenesis of HTLV-1, we will discuss the cellular and molecular mechanism of ATL generation from the virological point of view, particularly focusing on HBZ.
Highlights
Human T-cell leukemia virus type 1 (HTLV-1) is a complex retrovirus that infects approximately 10 to 20 million people worldwide [1]
The finding has suggested that individuals who possess MHC alleles which can efficiently bind and present peptides from HTLV-1 bZIP factor (HBZ) have significantly lower proviral load, and are less likely to develop HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) [16], suggesting that HBZ expression is a critical determinant of viral persistence in chronic phase of HTLV-1 infection
We have recently reported that the proportion of effector/memory CD4 T cells was increased in HBZ-transgenic (HBZ-Tg) mice [33], p30 p13
Summary
Human T-cell leukemia virus type 1 (HTLV-1) is a complex retrovirus that infects approximately 10 to 20 million people worldwide [1]. Thereafter, HTLV-1 was identified in a cell line derived from a patient with cutaneous T-cell leukemia in 1980 [3]. HTLV-1 has been shown to immortalize human T-lymphocytes in vitro [4]. The entire HTLV-1 sequence was determined [9] and various approaches were used to elucidate the pathogenesis of the virus. Recent studies have provided emerging evidence of the significance of HBZ in HTLV-1 pathogenesis. We discuss the present understanding of HTLV-I infection from the virological aspect via focusing on the role of the HBZ gene
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