Institut Cochin, Département de biologie cellulaire, 22, rue Méchain, 75014 Paris, Université américaine de Beyrouth, Département de médecine interne, Beyrouth, Liban
- Key words: retrovirus, leukemia, NF-kappaB, ubiquitin, SUMO
- DOI : 10.1684/vir.2007.0089
- Page(s) : 195-205
- Published in: 2007
HTLV-1 is a human retrovirus responsible for adult T-cell leukemia-lymphoma, a monoclonal proliferation of CD4 + T lymphocytes. In addition to the genes encoding the structural proteins and enzymes, the HTLV-1 genome encodes non structural proteins that regulate viral expression as well as various cellular machineries. Among them, Tax has rapidly been identified as the protein responsible for HTLV-1 transforming properties. Tax promotes cell proliferation by activating or repressing cellular genes and by disturbing the mechanisms that control cell division, DNA integrity and apoptosis. These multiple functions rely on the ability of Tax to recruit cytoplasmic and nuclear proteins. The mechanisms involved in the targeting of Tax toward these subcellular sites are still incompletely understood. This review describes the recent data concerning the intracellular maturation of Tax and the control of its functions through post-translational modifications.