Submitted March 6, 2006
Accepted June 27, 2006
HBZ, a new important player in the mystery of Adult-T-
cell leukemia
Jean-Michel MESNARD, Benoit BARBEAU, and Christian DEVAUX*
CNRS UMR5121-Universite Montpellier, France
Universite du Quebec a Montreal, Canada
* Corresponding author; email: christian.devaux{at}univ-montp1.fr.
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 80's. Over the years, many aspects of HTLV-1-induced 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 (Gaudray et al., J Virol. 2002;76:12813) and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology. Recently, four studies (Arnold et al., Blood. 2006;107:3976; Satou et al., Proc Natl Acad Sci USA 2006;103:720; Murata et al., J Virol. 2006;80:2495; Cavanagh et al., Retrovirology 2006;3:15) reported on the existence of different HBZ isoforms and have investigated on their function in both ATL cells or animal models. One report suggest 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.
