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How AIDS destroys immunity

A human gene named ATR normally protects people by preventing the replication of cells damaged by radiation or toxic chemicals. Now, Utah and New York researchers have discovered how a gene in the AIDS virus hijacks the human gene and turns it into a weapon that prevents reproduction of immune-system white blood cells, leaving AIDS patients vulnerable to deadly infections and cancer.

The new study "puts us a big step closer to understanding how HIV [human immunodeficiency virus] dismantles the immune system," says molecular biologist Vicente Planelles, an associate professor of pathology at the University of Utah School of Medicine.

It also raises the prospect for new kinds of treatments for AIDS and cancer.

Researchers already knew that an HIV gene named vpr led to the depletion of immune-system white blood cells named CD4+ lymphocytes. The new study suggests vpr does that by activating the ATR gene, which is found in white blood cells and all human cells.

The ATR gene's normal job is to detect genetic damage to cells caused by radiation, toxic chemicals and chemotherapy, and to stop the damaged cells from replicating until they can repair themselves. Planelles and researchers at the University of Rochester, N.Y., found evidence that the vpr gene one of nine genes in the AIDS virus exploits this normal repair process to stop vital white blood cells from replicating, thus disabling the immune system.

The findings were published last month in The Journal of Biological Chemistry.

The study raises the possibility of treating AIDS-related immune-system damage with medicines that prevent the human ATR gene from being activated by HIV's vpr gene.

"We would like to find a method or a substance that would allow us to interfere with the ability of HIV to kill the white blood cells using this mechanism," Planelles says.

It may take five to 10 years to develop medicines to interfere with the human ATR ge
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Contact: Vicente Planelles
vicente.planelles@path.utah.edu
801-581-8655
University of Utah Health Sciences Center
20-Aug-2003


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