AIDSWEEKLY Plus; Monday, October 15, 2001
Michael Greer, Senior Medical Writer
NewsRx -- Researchers in the United States say that genotypes linked to reduced function of the CCR5 coreceptor, used by most HIV strains for cell entry, appear to confer a natural resistance to HIV infection.
Michael Marmor and colleagues at the New York University School of Medicine, the New York Blood Center, the California Department of Health Services in Berkeley, the San Francisco Department of Public Health, Harvard University in Boston, Abt Associates, a consulting firm in Cambridge, Massachusetts, and the Fred Hutchinson Cancer Research Center in Seattle conducted a study to "investigate evidence for resistance to HIV-1 infection associated with the heterozygous genotype CCR5-+/ (delta) 32 and the homozygous genotype CCR5- (delta) 32/ (delta) 32, which results in a nonfunctional CCR5 receptor."
Even CCR5 (delta) 32 heterozygotes were markedly more resistant to HIV infection than individuals with normal CCR5 genes, Marmor and coworkers found.
The researchers examined data from almost 3000 study participants in eight American cities. Caucasian gay or bisexual men who engaged in high-risk sexual activities were significantly (P=0.002) more likely to have CCR5 (delta) 32 heterozygotes, indicating a "selective advantage" for this genotype among this population, they said.
Marmor and team also calculated the relative risk of contracting HIV infection for different populations, adjusted for high-risk behavior such as unprotected anal sex. This analysis revealed that CCR5 (delta) 32 heterozygote individuals were more than three times less likely to become infected than individuals with normal genotypes, study data showed.
The homozygous CCR5 (delta) 32 genotype was also linked to reduced HIV risk, being significantly more common among older study participants in cities with a high prevalence of HIV infection but not in low-prevalence cities ("Homozygous and heterozygous CCR5- (delta) 32 genotypes are associated with resistance to HIV infection," J Acquir Immune Defic Syndr 2001 Aug 15;27(5):472-81.
"These findings imply that strategies aimed at reducing susceptibility to HIV infection by blocking CCR5 receptor sites need not seek blockage of all receptor sites to achieve an imperfect but substantial degree of protection," Marmor and colleagues concluded.
The corresponding author for this report is Michael Marmor, New York University School of Medicine, Dept. of Environmental Medicine, 650 1st Avenue, 5th Floor, New York, NY 10016, USA.
Key points reported in this study include:
This article was prepared by AIDS Weekly editors from staff and other reports.
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