CCR5 genotype and HIV-1 infection in perinatally-exposed infants.
The CCR5 chemokine receptor is required by non-syncytium HIV-1 strains to infect target cells. A 32 base pair deletion (delta32) in the CCR5 gene causes a structural CCR5 modification that does not permit HIV-1 entry into cells. The rate of the CCR5 delta32 was investigated in 137 children born from HIV-infected mothers. Overall, five (10.6%) of 47 HIV-infected infants showed the defect in heterozygosis vs. eight (8.9%) of 90 uninfected children. No CCR5 delta32 homozygotes were found. Interestingly, among infected children, five (21.7%) of 23 showing a slow disease progression were heterozygous for the CCR5 delta32, meanwhile none of the 24 infants with rapid disease course had the deletion (P = 0.022). In conclusion, the CCR5 delta32 defect does not protect against vertical HIV-1 transmission, but is associated with a delayed disease progression in HIV-infected children.
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Servicio de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain.
Español
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Heredia
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A
Pedraza
M A
MA
Hernandez
M
M
Caragol
I
I
Fernando
M
M
Bertran
J M
JM
Alcami
J
J
Soriano
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V
D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D015497:HIV-1 / Q000472:pathogenicity*; D006579:Heterozygote; D006801:Humans; D007231:Infant, Newborn; D018445:Infectious Disease Transmission, Vertical; D019656:Loss of Heterozygosity; D011247:Pregnancy; D019713:Receptors, CCR5 / Q000235:genetics*; D017384:Sequence Deletion / Q000235:genetics; D044465:White People / Q000235:genetics
D019713:Receptors, CCR5