Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
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Reuters NewMedia, Inc. - 26 September 1996
Joanne Kenen
Scientists have long sought to understand why some people exposed to the HIV virus do not become infected. They are eager to identify any natural defenses against AIDS, in the hope that they can gain further insight into the disease and develop new therapies or vaccines to treat or prevent it.
In research appearing Friday in the journal Science, a team at the National Cancer Institute (NCI) took the recent findings about the CKR5 gene and linked it to data on AIDS gathered in six major epidemiological studies nationwide.
``We entered into a collaboration with a number of epidemiologist who have been tracking HIV exposed and infected patients for the last 15 years,'' lead researcher Stephen O'Brien of the NCI said in an interview.
The HIV virus infects a cell in a multi-step process. It must grab onto the cell, and then it must penetrate it. The CKR5 defect, discovered just months ago, interrupts that penetration process in white blood cells known as macrophages.
Looking at health history data on 1955 people, scientists confirmed that not one of the 17 people who had two copies of the defective CKR5 gene, one inherited from each parent, had developed AIDS despite exposure to the HIV virus.
The findings provide only a piece of the puzzle, however, O'Brien cautioned. There were 622 people in the studies who were not HIV infected despite high risk of exposure, or repeated exposure. But only 17 had this dual genetic defect.
``We explained three percent of the cases. We still have to find out about the other 97,'' he said.
The researchers also found that a single copy of the gene defect did not provide immunity. Of the 282 people who had one altered copy of the gene, about two-thirds were HIV-infected.
But homosexual males with one defective CKR5 gene who were HIV infected tended to live two or three years longer before developing AIDS symptoms than those without a defect.
But for reasons not yet understood, hemophiliacs with the same single copy defect were less likely to progress slowly.
The genetic defect was much more common among U.S. whites than among U.S. blacks, the scientists found. Based on the research done so far, it has not been seen in African blacks.
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