Polymorphisms in the CCR5 Promoter Region Influence Disease Progression in Perinatally Human Immunodeficiency Virus Type 1–Infected Children
Copyright policy )Polymorphisms in the CCR5 Promoter Region Influence Disease Progression in Perinatally Human Immunodeficiency Virus Type 1–Infected Children
The effect of CC-chemokine receptor 5 (CCR5) promoter polymorphisms on the natural history of human immunodeficiency virus (HIV) disease was studied in 73 HIV-1-infected children. The CCR5(59338-59537) promoter haplotype, CCR5-59029A/G polymorphism, and CCR5Delta32 and CCR2-64I alterations were investigated. After exclusion of carriers of CCR5Delta32 or CCR2-64I, Kaplan-Meier analysis disclosed that children with the P1/P1(59353C,59356C,59402A) genotype progressed faster to disease than did children with other haplotypes (P=.016). When CCR2-64I carriers were included, this effect had borderline significance (P=.065) and was lost when CCR5Delta32 carriers were also considered (P=.387). The P1/P1 effect was strongest early after infection, when progression to disease was mainly associated with CCR5 coreceptor-using viruses. These results indicate that the P1/P1 genotype is predictive of rapid progression in HIV-1-infected children lacking CCR5Delta32 or CCR5-64I alleles. The observation of a linkage disequilibrium between P1 and 59029A might explain the previously reported association between 59029A homozygosity and rapid disease progression.
- University of Padua Italy
Adult, Male, Polymorphism, Genetic, Adolescent, Age Factors, Infant, Newborn, Infant, HIV Infections, Infectious Disease Transmission, Vertical, Linkage Disequilibrium, Perinatal Care, Haplotypes, Child, Preschool, Disease Progression, HIV-1, Humans, Point Mutation, Female, Child, Alleles
Adult, Male, Polymorphism, Genetic, Adolescent, Age Factors, Infant, Newborn, Infant, HIV Infections, Infectious Disease Transmission, Vertical, Linkage Disequilibrium, Perinatal Care, Haplotypes, Child, Preschool, Disease Progression, HIV-1, Humans, Point Mutation, Female, Child, Alleles
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