blood cells called CD4+ and CD8+ T cells, but only the CD4+ subset becomes leukemic. To better understand why, researchers Eric Wattel and colleagues at the Universit Claude Bernard in France isolated T cells from patients with HAM/TSP. The authors found that although both subsets of HTLV-1infected T cells had higher growth rates than uninfected cells, the mechanisms were different: while CD4+ cells were recruited to enter an active process of cell division called the cell cycle, CD8+ cells were prevented from dying. In addition, although the HTLV-1 viral protein called "tax" was present in both subsets of infected cells, only CD4+ T cells displayed abnormalities in their appearance and defects in a type of cell division called cytokinesis. Thus, the effects of HTLV-1 infection are distinct for each T cell subset. Further study showed that the increased cell cycling (as seen in infected CD4+ cells), but not the reduction in cell death (as seen in infected CD8+ cells), correlated with tax levels, suggesting that tax is a critical determinant of the sensitivity of CD4+ cells to leukemia. The study appears in the April issue of the Journal of Clinical Investigation.
In an accompanying commentary, O. John Semmes from Eastern Virginia Medical School in Norfolk, writes that this study will allow researchers to better identify a postinfection, nonmalignant cell-based on some of the cell's behavior. He further notes that, "the determination of the molecular events that occur between virus infection and disease development has been a particularly challenging area of research."
TITLE: HTLV-1 propels untransformed CD4+ lymphocytes into the cell cycle while protecting CD8+ cells from death
AUTHOR CONTACT: Eric Wattel
Universit Claude Bernard, Lyon Cedex, France
Phone: 33-478-78-26-69; Fax: 33-478-78-27-17; E-mail: wattel@lyon.fnclcc.fr
View the PDF of this article at:
Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
3-Apr-2006
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