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J Biol Chem, Vol. 273, Issue 12, 6698-6703, March 20, 1998

A Human T-cell Leukemia Virus Tax Variant Incapable of Activating NF-B Retains Its Immortalizing Potential for Primary T-lymphocytes

Oliver Rosin, Claudia Koch, Iris Schmitt, O. John Semmes^§, Kuan-Teh Jeang^§, and Ralph Grassmann

From the  Institut für Klinische und Molekulare Virologie, Universität Erlangen-Nürnberg, Schloßgarten 4, D-91054 Erlangen, Federal Republic of Germany and ^§ Molecular Virology Section, NIAID, National Institutes of Health, Bethesda, Maryland 20892-0460

The human T-cell leukemia virus type 1 (HTLV-1) transactivator (Tax) has been shown to interfere with regulated cellular proliferation. Many studies have focused on the ability of Tax to transform rodent fibroblasts; however, none has defined the molecular requirements for Tax transformation of human lymphoid cells. We show here that tax induces permanent growth of human primary T-lymphocytes by using a transformation/immortalization defective rhadinovirus vector. The cells phenotypically resemble HTLV-immortalized lymphocytes and contain episomally persisting recombinant rhadinoviral sequences, which stably express functional Tax protein. As Tax can activate major cellular signal transducing pathways including NF-B and cAMP-responsive element binding protein (CREB), we asked for the relevance of these routes in the immortalization of human lymphocytes. By using Tax mutants that either activate exclusively CREB/activating transcription factor or are defective in activating this signaling pathway, we delineated that Tax can induce immortalization of primary human T-lymphocytes through a mechanism independent of NF-B activation.

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