The human T-cell leukemia viruses (HTLV) are associated with T-cell malignancies in humans. The malignant transformation occurs after a long latency in some carriers, and its mechanism appears to be distinct from that of other classes of retroviruses which induce transformation through viral or cellular oncogenes. A widely postulated explanation is that the products of novel pX genes transactivate endogenous cellular genes which lead to tumor development in T cells. To directly examine the pathological effects of pX genes in vivo, we produced transgenic mice harboring the HTLV type I pX genes under several regulatory units: HTLV type I long terminal repeat, immunoglobulin enhancer-simian virus 40 promoter, and mouse mammary tumor virus long terminal repeat. Atrophy of the thymus was characteristic in these mice no matter which regulatory unit directed the expression of the genes.

Animal Atrophy Cell Transformation, Neoplastic *Genes, Viral HTLV-I/GENETICS/ISOLATION & PURIF/*PATHOGENICITY Mice Mice, Transgenic Thymus Gland/*MICROBIOLOGY/PATHOLOGY Thymus Neoplasms/*MICROBIOLOGY/PATHOLOGY JOURNAL ARTICLE

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