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The method by which a key HIV gene stops immune system cells from replicating has been identified by researchers at the University of Utah and the University of Rochester, reports Scripps Howard News Service. Laboratory tests showed that the viral gene, called VPR, activates a usually dormant gene inside of T cells that, when stimulated, prevents the cells from regenerating. Low T-cell levels are a hallmark of HIV disease, with very low levels resulting in immune system damage that can permit opportunistic infections to take hold. The researchers say new treatments may be developed that prevent the VPR gene from activating the cellular genes, which could prevent such immune system damage. "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," said researcher Vincente Planelles of the University of Utah. But the researchers say developing such a treatment could take between five and 10 years. Earlier this year, researchers at the Mayo Clinic in Rochester, Minn., reported that damage or mutations to VPR can slow the virus's ability to destroy immune system cells and that many HIV nonprogressors, the name given to HIV-positive people who never develop AIDS, carry HIV with damaged versions of the gene. Although HIV was still able to slowly kill immune system cells in these patients, their bodies were able to replenish T-cell supplies quickly enough to prevent serious immune deterioration. "Since mutations in VPR can alter the outcome of HIV disease, it is possible, if not likely, that we can develop inhibitors of VPR that may also modify disease outcome," said lead researcher Andrew Badley.
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