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12th International AIDS ConferenceGeneva, Switzerland - June 28-July 3, 1998 |
Int Conf AIDS 1998 Jun 28-Jul 3; 12:4 (abstract no. 11108)
Kemeny B, Nagy K, Horuath A
Natl Inst of Derm-Vener, Budapest, Hungary.
OBJECTIVES: CCR5 is a chemokine receptor and also serves as co-receptor for non-syncitia inducing, macrophage-tropic strains of HIV. It had been shown that a 32 base-pair deletion in the gene results in a severely truncated protein and leads to a partial resistance in HIV infection. As the majority of the sexually transmitted HIV-1 isolates are macrophage-tropic, we studied the polymorphism of the CCR5 gene in our HIV infected patients as well as in normal population.
METHODS: The following groups were included in our study: long-term non progressor (LTNP) HIV-infected individuals, HIV-infected persons with usual progression of infection, their sexual contacts, and healthy individuals. The analysis was done by PCR of DNA isolated from PBMCs of the patients.
RESULTS: Out of 117 determinations, heterozygote mutations of the CCR5 gene were demonstrated in 40% of the LTNPs, in 16% of HIV progressors, in 17% of the HIV negative contacts and 21% of healthy individuals. Homozygous form of A32 deletion has been found in two cases (1.9%), none of them were infected by HIV. Allele frequency of the deletion is 0.120.
CONCLUSIONS: The high prevalence of Δ32 deletion of CCR5 gene among LTNPs supports findings, that mutation in co-receptor gene may provide a certain protection against HIV infection and/or contribute to the delayed progression of AIDS.
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