Abstract
The mechanism of cellular transformation by the human T-cell leukemia viruses (HTLV) is thought to involve a novel gene known as the x gene. This gene is essential for HTLV replication and acts by enhancing transcription from the HTLV long terminal repeat. The HTLV x gene product may also cause aberrant transcription of normal cellular genes, resulting in transformation of the infected cells. Although there is no evidence as yet for such a mechanism, it was shown that the HTLV-II x gene product can activate transcription from adenovirus E1A-dependent early promoters and therefore has the potential to activate cellular genes. It was also shown that the adenovirus and herpes pseudorabies immediate early proteins activate expression from the HTLV-I and HTLV-II long terminal repeats, though at lower levels than with the x gene product. These findings indicate possible common mechanisms of action for transcription-regulatory genes of distinct viruses.
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