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FAT10: a Novel Mediator of Vpr-Induced Apoptosis in Human Immunodeficiency Virus-Associated Nephropathy
Journal of Virology, 10/28/09

Snyder A et al. – The authors found that Vpr interacts with FAT10 and that these proteins colocalize at mitochondria. These studies establish FAT10 as a novel mediator of Vpr–induced cell death.

Exclusive Author Commentary
Michael J. Ross, 11/02/09

In this manuscript we identify the ubiquitin-like protein FAT10 as an important mediator of HIV-1 Vpr induced apoptosis in human renal epithelial cells. Suppression of FAT10 expression was able to prevent Vpr-induced apoptosis with a corresponding increase in the proportion of hyperploid cells, suggesting that FAT10 expression facilitates apoptosis of cells with Vpr-induced hyperploidy. Further, we demonstrate that FAT10 and Vpr colocalize at mitochondria. Vpr is a critical mediator of HIV induced renal disease, and FAT10 has been previously shown to be upregulated in renal epithelial cells in patients with HIV-associated nephropathy. These studies therefore establish FAT10 as a potential therapeutic target for the prevention or treatment of HIV-associated renal disease.

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