AIDSWEEKLY Plus; Monday, December 14, 1998
Daniel J. DeNoon, Senior Editor
Several genetic variants have been found to offer various degrees of protection against AIDS. New findings by National Cancer Institute researchers Maureen P. Martin and colleagues are the first to identify an AIDS-accelerating gene.
The recessive gene is expressed as a variant of the CCR5 chemokine receptor, the key used by macrophage-tropic HIV strains in the vast majority of infections. In order to have increased susceptibility to AIDS a person must inherit the gene, called CCR5P1, from both parents. Unfortunately, this happens quite often.
"CCR5P1 represents the first allelic variant to accelerate AIDS progression, and 12.7 percent of Caucasians and 6.7 percent of African Americans carry a CCRP1/P1 genotype," Martin et al. observed.
The researchers reported their findings in the journal Science ("Genetic Acceleration of AIDS Progression by a Promoter Variant of CCR5," Science, 1998;282:1907-11).
People homozygous for the variant CCR5 gene develop AIDS with remarkable speed. Martin et al. calculated that the gene is responsible for 10 to 17 percent of AIDS cases that develop within 3.5 years of HIV infection.
As many as 13 percent of all people carry the AIDS-acceleration genotype.
Genotypes that offer some protection against HIV occur in nearly 40 percent of Caucasians and more than 30 percent of African Americans. The HIV-accelerating gene appears to be as powerful as the most highly protective of the protective genotypes, the CCR5-delta32 mutation.
Consistent with data showing that CCR5-dependent HIV strains predominate in early HIV infection, the effect of the CCR5P1 mutation exerts its strongest effects in the initial four to six years after infection.
"These findings may provide a basis for the development of therapeutic applications as well as for the resolution of other complex polygenic human diseases, including those that require environmental contingencies (such as viral exposure) for phenotype recognition," Martin et al. concluded.
This work was supported by the National Cancer Institute.
The corresponding author for this study is Stephen J. O'Brien, Laboratory of Genomic Diversity, National Cancer Institute, Frederick, Maryland 21702. Email: <obrien@ncifcrf.gov>.
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