Abstract
A deletion of 32 base pairs in the CCR5 gene (delta32 CCR5) has been linked to resistance to HIV-1 infection in exposed adults and to the delay of disease progression in infected adults. To determine the role of delta32 CCR5 in disease progression of HIV-1 infected children born to seropositive mothers, we studied a polymerase chain reaction in 301 HIV-1 infected, 262 HIV-1 exposed-uninfected and 47 HIV-1 unexposed-uninfected children of Spanish and Italian origin. Infected children were further divided into two groups according to their rate of HIV-1 disease progression: rapid progressors who developed severe clinical and/or immunological conditions within the second year of life, and delayed progressors with any other evolution of disease. Among the latter were the long-term, non-progressors (LTNP) who presented with mild or no symptoms of HIV-1 infection above 8 years of age. Viral phenotype was studied for 45 delayed progressors. No correlation was found between delta32 CCR5 and mother-to-child transmission of HIV-1. However, the frequency of the deletion was substantially higher in LTNP, compared with delayed (p = 0.019) and rapid progressors (p = 0.0003). In children carrying the delta32 CCRS mutation, the presence of MT-2 tropic virus isolate was associated with a severe immune suppression (p = 0.028); whereas, the presence of MT-2 negative viruses correlated with LTNP (p = 0.010). Given the rapidity and simplicity of the assay, the delta32 CCR5 mutation may be a useful predictive marker to identify children with delayed disease progression who, consequently, may not require immediate antiretroviral treatment.
Highlights
More than 90% of Human Immunodeficiency Virus type 1 (HIV-1) infection in children is acquired by mother-to-child transmission [1]
We show that the presence of the ⌬32 CCR5 mutation, either heterozygous or homozygous, is not associated with transmission of HIV-1 from the mother to the child
Misrahi et al [20] described only one homozygous carrier of the ⌬32 CCR5 mutation, an uninfected child, in a cohort of 512 French children born to HIV-1 positive mothers
Summary
More than 90% of Human Immunodeficiency Virus type 1 (HIV-1) infection in children is acquired by mother-to-child transmission [1]. The heterozygous form of the mutation has been correlated with delayed disease progression in HIV-1 infected adults [15,16]. Infected children were further divided into two groups according to their rate of HIV-1 disease progression: rapid progressors who developed severe clinical and/or immunological conditions within the second year of life, and delayed progressors with any other evolution of disease. Among the latter were the long–term, non–progressors (LTNP) who presented with mild or no symptoms of HIV-1 infection above 8 years of age. Conclusions: Given the rapidity and simplicity of the assay, the ⌬32 CCR5 mutation may be a useful predictive marker to identify children with delayed disease progression who, may not require immediate antiretroviral treatment
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