A human T lymphotropic virus type I (HTLV-I) long terminal repeat-directed antisense c-mycconstruct with an Epstein-Barr virus replicon vector inhibits cell growth in a HTLV-I-transformed human T cell line

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Abstract
A panel of EB virus replicon‐based vectors was constructed to examine the relative utility of four distinct eukaryotic promoters for high‐level gene expression in a HTLV‐I‐transformed human T cell line, HUT102. We found that HTLV‐I LTR, which is trans‐activated by the viral tax protein, was most suited for EBV vector‐based stable gene expression in it. We prepared a HTLV‐I LTR‐directed antisense c‐myc construct with an EBV vector. This antisense plasmid suppressed c‐myc expression and inhibited growth of HUT102 cells in vitro with unaltered expression of tax. Non‐specific plasmid toxicity was excluded by showing that the antisense construct had little effect on growth and c‐myc expression of HTLV‐I‐negative Jurkat T cells, in which the viral LTR is expected to be less active. Our results indicate that c‐myc may play an important role in the deregulated growth of HTLV‐I‐transformed T cells.