CCR5 genotype and HIV-1 infection in perinatally-exposed infants

• Published in: The Journal of infection Vol. 38; no. 1; pp. 9 - 11
• Main Authors: Mas, A., Español, T., Heredia, A., Antonia Pedraza, M., Hernandez, M., Caragol, I., Fernando, M., Bertran, J.M., Alcami, J., Soriano, V.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 1999; Elsevier
• Subjects: AIDS/HIV; Biological and medical sciences; European Continental Ancestry Group - genetics; Female; Genotype; Heterozygote; HIV Infections - etiology; HIV Infections - genetics; HIV Infections - pathology; HIV-1 - pathogenicity; Human immunodeficiency virus 1; Human viral diseases; Humans; Infant, Newborn; Infectious Disease Transmission, Vertical; Infectious diseases; Loss of Heterozygosity; Medical sciences; Pregnancy; Receptors, CCR5 - genetics; Sequence Deletion - genetics; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Human; Immunopathology; Prognosis; Typing; HIV-1 virus; Retroviridae; Genotype; Infant; AIDS; Immune deficiency; Lentivirus; Infection; Virus; Chemokine; Viral disease; Risk factor; Deletion; Evolution; Vertical transmission; Human immunodeficiency virus; Biological receptor
• ISSN: 0163-4453; 1532-2742
• DOI: 10.1016/S0163-4453(99)90020-8

The CCR5 chemokine receptor is required by non-syncytium HIV-1 strains to infect target cells. A 32 base pair deletion (Δ32) in the CCR5 gene causes a structural CCR5 modification that does not permit HIV-1 entry into cells. The rate of the CCR5 Δ32 was investigated in 137 children born from HIV-infected mothers. Overall, five (10.6%) of 47 HIV-infected infants showed the defect in heterozygosi vs. eight (8.9%) of 90 uninfected children. No CCR5 Δ32 homozygotes were found. Interestingly, among infected children, five (21.7%) of 23 showing a slow disease progression were heterozygous for the CCR5 Δ32, meanwhile none of the 24 infants with rapid disease course had the deletion (
P = 0.022). In conclusion, the CCR5 Δ32 defect does not protect against vertical HIV-1 transmission, but is associated with a delayed disease progression in HIV-infected children.