Immune reconstitution in human immunodeficiency virus-infected children receiving highly active antiretroviral therapy: a cohort study.


Journal Article

BACKGROUND: Highly active antiretroviral therapy (HAART) has brought about rapid declines in HIV-1 RNA concentrations and an increase in CD4+ counts in HIV-1-infected children. These changes are often accompanied by clinical improvement; however, the extent to which immune reconstitution occurs is not known. DESIGN: We compared two cohorts (n = 35) of HIV-1-infected children to evaluate the effects of HAART on immune recovery. Cohort 1 (C1) included clinically well children receiving HAART with a CD4 >22% at study initiation. Before HAART all children had moderately to severely suppressed immune function by CDC criteria (CD4 <25%) or CDC Category B or C disease. Cohort 2 (C2) included children with no current or past evidence of immunosuppression based on CDC criteria (CD4 >25%) and no evidence of clinical disease. Children in C2 were receiving a non-HAART regimen. METHODS: Immunophenotyping was performed to characterize CD4+ and CD8+ subsets with regard to maturation and activation. T cell rearrangement excision circles (TRECs) were measured to quantify recent thymic emigrants. RESULTS: No difference was found in percent CD4+ or percent CD8+ T cells or maturation markers between C1 and C2. There was significantly less expression of activation markers in both CD4+ and CD8+ cells in C1. There was no difference in TREC production between C1 and C2. CONCLUSION: Moderately to severely suppressed HIV-1-infected children receiving HAART are able to reconstitute their immune systems to a degree that is indistinguishable from that of stable, CDC Class A1 HIV-1-infected children with regard to CD4+ and CD8+ T cell subsets, expression of cellular maturation markers and TREC production.

Full Text

Duke Authors

Cited Authors

  • Johnston, AM; Valentine, ME; Ottinger, J; Baydo, R; Gryszowka, V; Vavro, C; Weinhold, K; St Clair, M; McKinney, RE

Published Date

  • October 1, 2001

Published In

Volume / Issue

  • 20 / 10

Start / End Page

  • 941 - 946

PubMed ID

  • 11642627

Pubmed Central ID

  • 11642627

International Standard Serial Number (ISSN)

  • 0891-3668

Digital Object Identifier (DOI)

  • 10.1097/00006454-200110000-00006


  • eng

Conference Location

  • United States