Abstract
HTLV-1 is etiologically implicated with adult T-cell leukemia (ATL) and tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). Neither of them is curable by presently known therapy. Therefore, both disorders are waiting for novel therapeutic approaches. Developing such approaches requires comprehensive insight into the viral and cellular factors involved in the genesis of these diseases. It is widely accepted that the viral Tax protein plays a key role in initiating the process leading to ATL, as well as in the pathogenesis of TSP/HAM. Therefore, its various activities are attractive targets for novel molecular or/and immunological therapies. This review describes the effects of Tax that confer its oncogenic potential. These effects require a sufficiently high level of Tax protein, whereas shortly after human infection, the virus enters into a latent state in which no or very low viral gene expression and Tax protein can be detected in the infected cells of the virus carriers. This implies that the dormant virus must be activated in order to elevate Tax
Keywords: HTLV-1, Tax, ATL, TSP/HAM, genetic instability, apoptosis