Prognostic value of a CCR5 defective allele in pediatric HIV-1 infection

M L Romiti1, C Colognesi, C Cancrini

  • 1Division of Immunology and Infectious Diseases, Children's Hospital Bambino Gesù, University of Rome Tor Vergata, Italy.

Insights

The CCR5 delta32 gene deletion is linked to slower HIV-1 disease progression in children. This genetic marker may help identify children who do not need immediate antiretroviral treatment.

Area of Science:

  • Immunology
  • Genetics
  • Virology

Background:

  • The CCR5 delta32 gene deletion is associated with reduced HIV-1 infection risk and delayed disease progression in adults.
  • Understanding this mutation's role in pediatric HIV-1 is crucial for disease management.

Purpose of the Study:

  • To investigate the impact of the CCR5 delta32 gene deletion on HIV-1 disease progression in children.
  • To assess the CCR5 delta32 mutation's correlation with mother-to-child HIV-1 transmission and disease outcomes.

Main Methods:

  • Polymerase chain reaction was used to genotype 301 HIV-1 infected, 262 HIV-1 exposed-uninfected, and 47 HIV-1 unexposed-uninfected children.
  • HIV-1 infected children were classified as rapid or delayed progressors, including long-term non-progressors (LTNP).
  • Viral phenotype analysis was performed on 45 delayed progressors.

Main Results:

  • No association was found between CCR5 delta32 and mother-to-child HIV-1 transmission.
  • The CCR5 delta32 deletion was significantly more frequent in long-term non-progressors (LTNP) compared to delayed and rapid progressors.
  • In children with the CCR5 delta32 mutation, MT-2 tropic viruses correlated with severe immune suppression, while MT-2 negative viruses correlated with LTNP status.

Conclusions:

  • The CCR5 delta32 mutation is associated with delayed HIV-1 disease progression in children.
  • The CCR5 delta32 mutation may serve as a predictive marker for identifying children with slower disease progression.
  • Identifying children with delayed progression could help guide decisions regarding the initiation of antiretroviral therapy.
Abstract

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