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Virologic and host characteristics of human immunodeficiency virus type 1-infected pediatric long term survivors

Louis Alexander1, Lisa Cuchura, B Joyce Simpson

  • 1Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College Street, New Haven, CT 06520, USA. louis.alexander@yale.edu

The Pediatric Infectious Disease Journal
|February 8, 2006
PubMed

Insights

Host and viral factors, not just limited treatment, contribute to slow human immunodeficiency virus type 1 (HIV-1) progression in children. Genetic factors like CCR2 polymorphism and viral mutations appear crucial for long-term non-progressive HIV-1 infection.

Area of Science:

  • Pediatric Infectious Diseases
  • Virology
  • Immunogenetics

Background:

  • Limited data exists on factors influencing varying clinical progression rates in pediatric human immunodeficiency virus type 1 (HIV-1) infection.
  • Understanding these determinants is crucial for managing HIV-1 in children.

Purpose of the Study:

  • To investigate whether viral and host factors known to be associated with nonprogressive HIV-1 infection in adults are also present in children with minimal disease progression.
  • To identify potential mechanisms contributing to long-term non-progressive HIV-1 infection in vertically infected youths receiving minimal antiretroviral therapy.

Main Methods:

  • Characterization of 5 vertically HIV-1 infected youths (ages 12-18) with minimal disease progression and low antiretroviral exposure.
  • Analysis of plasma HIV-1 RNA loads, CD4 T-lymphocyte counts/percentages.
  • Sequencing of predominant HIV-1 strains to identify resistance markers and replication-inhibiting mutations (Gag, Vif).
  • Genotyping for CCR2 polymorphism (64I) and analysis of histocompatibility leukocyte antigen (HLA) phenotypes (DQ1, DR/DQ1).

Main Results:

  • All 5 long-term survivors maintained low HIV-1 RNA levels and normal CD4 counts.
  • 4 out of 5 harbored HIV-1 with therapy resistance markers; 2 had viral isolates with Gag/Vif insertions inhibiting replication.
  • 2 individuals were heterozygous for CCR2 64I polymorphism, associated with slower AIDS progression in adults.
  • All 5 expressed HLA DQ1, with 2 showing unusual DR/DQ1 phenotypes.

Conclusions:

  • Limited antiretroviral therapy alone does not explain the benign clinical status of these long-term survivors.
  • Host genetic factors (e.g., CCR2 polymorphism, HLA types) and viral characteristics (e.g., reduced replicative capacity) likely contribute to controlling HIV-1 progression.
  • No single virologic or host factor fully explains the non-progressive phenotype in all cases, suggesting a multifactorial etiology similar to adults.
Abstract

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