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Blood, 15 December 2006, Vol. 108, No. 13, pp. 3979-3982. Prepublished online as a Blood First Edition Paper on August 17, 2006; DOI 10.1182/blood-2006-03-007732.
PERSPECTIVES HBZ, a new important player in the mystery of adult T-cell leukemiaFrom the Laboratoire Infections Rétrovirales et Signalisation Cellulaire, Centre National de la Recherche Scientifique (CNRS) Unité mixte de recherche (UMR) 5121-UM1, Montpellier, France; and the Département des Sciences biologiques, Université du Québec à Montréal, Canada.
Abstract Adult T-cell leukemia (ATL) was first described in 1977. A link between ATL and human T-cell leukemia virus type 1 (HTLV-1) was clearly established in the early 1980s. Over the years, many aspects of HTLV-1induced cellular dysfunctions have been clarified. However, the detailed mechanism behind ATL occurrence remains unsolved. Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-cell transformation) in more than 50% of ATL cells. A novel HTLV-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology. Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both ATL cells or animal models. One report suggests that the HBZ gene might have a bimodal function (at the mRNA and protein levels), which could represent an uncharacterized strategy to regulate viral replication and proliferation of infected T cells.
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