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Mutated Gene Common in Whites Discovered to Slow Effects of HIV

By Rick Weiss
The Washington Post
WASHINGTON

A genetic mutation common in U.S. whites slows the progression of AIDS in people infected with the AIDS-causing virus, and in some cases protects individuals against the disease, according to a new study.

Scientists said the new information on the role played by the defective gene could lead to advances in the fight against AIDS by spurring the development of medicines or vaccines that mimic the protective mutation's effects.

"It's a beautiful study," said Robert C. Gallo, head of the University of Maryland's Institute of Human Virology in Baltimore, who in 1984 co-discovered the human immunodeficiency virus.

The new work shows that about 1 in 7 U.S. whites and about 1 in 59 U.S. blacks inherit the protective, mutant gene from one parent, along with a normal copy of the gene from the other parent. This harmless genetic condition naturally slows the progress of AIDS, giving an average of three extra years of life to those infected with HIV, according to the study in today's issue of Science.

The study also confirms previous hints that about 1 percent of American whites inherit a mutant version of the gene from both parents - a doubly protective dose that makes these individuals virtually impervious to infection even if they are repeatedly exposed to the virus.

The new research, led by the National Cancer Institute's Stephen J. O'Brien, Michael Dean and Mary Carrington, helps explain why some people exposed to HIV fare better than others. It also shows that the protective mutation is rare in African blacks, which suggests that the genetic glitch may have arisen in an ancestral Caucasian after the two races diverged.

Researchers praised the findings as an example of the benefits that can accrue from the dogged and unglamorous work of community-based AIDS organizations, which have for more than a decade collected blood samples from thousands of HIV-infected people and kept track of each individual's fate. It was through the NCI team's genetic analysis of those samples, that the naturally occurring protective factors were found.

"It's the extensive epidemiological data collected on these patients that made this work possible," said O'Brien, who directs NCI's laboratory of genomic diversity in Frederick, Md.

The work is the latest in a rapid-fire series of discoveries since June that has shifted AIDS researchers' attention away from the virus itself and onto a protein studding the surface of some human cells.

The protein, known as CKR5 or CCR5, is part of a portal system that allows the AIDS virus to enter cells of the immune system. People with mutant CKR5 genes cannot make the crucial portal protein, and hence are protected to varying extents from viral invasion.

The researchers focused on the CKR5 gene, which carries instructions for making a protein on macrophages, the white blood cells that HIV initially infects. That protein serves as a docking site for an immune system hormone, but the AIDS virus can usurp the site to infect macrophages.

No one knows what that disease was, or whether it still exists. "It probably wasn't AIDS," O'Brien said. "But whatever it was, it probably had a high mortality."