Human T lymphotropic virus type-I (HTLV-I), the causative agent of adult T cell leukaemia (ATL), is the only human retrovirus known to cause malignancy. Molecular studies of HTLV-I have revealed a complex mechanism regulating viral gene expression. This mechanism involves the control of mRNA expression at both the transcriptional and post-transcriptional levels, by the viral gene products Tax and Rex, respectively. In addition to transactivating the viral long terminal repeat promoter, Tax activates numerous cellular genes, and thus is strongly implicated in the initial stages of cell transformation. However, the subsequent genetic events leading to the fully transformed phenotype found in ATL remain to be elucidated. Present models of HTLV-I- induced neoplasia propose the involvement of additional viral factors or secondary events leading to the emergence of clones with a selective growth advantage. Given the long latency period between HTLV-I infection and the clinical manifestations of ATL, considerable effort is currently focused on the development of animal models reproducing ATL in a time course more suitable for experimental studies of the interplay between HTLV-I gene products and the host cell machinery.
|Number of pages||19|
|Journal||FORUM - Trends in Experimental and Clinical Medicine|
|Publication status||Published - 1994|
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