Protease inhibitor and triple-drug therapy: cellular immune parameters are not restored in pediatric AIDS patients after 6 months of treatment

AIDS. 1998 Dec 24;12(18):2397-406. doi: 10.1097/00002030-199818000-00008.

Abstract

Objective: To assess whether treatment of HIV-positive children by antiretroviral drugs for a 6-month period would improve immune function significantly.

Design and methods: Immunological assessment of 89 HIV-positive children who received protease inhibitor monotherapy for 12-16 weeks as part of phase I/II studies, followed by triple antiretroviral therapy for an additional 12 weeks, was conducted. Immunological parameters were assessed in vitro at four time points (at enrollment, at weeks 2-4, at weeks 12-16, and at weeks 24-28). Assessments included: cytokine production by monocytes, T-cell proliferation to mitogen or recall antigens (including an HIV antigen) and apoptotic cell death. Plasma levels of tumor necrosis factor (TNF)-alpha and soluble TNF receptor (sTNF-R) were also measured, in addition to CD4+ T-lymphocyte counts and viral load. In addition, limited analyses were performed on samples from 17 children after 120 weeks of therapy, including 104 weeks of triple therapy.

Results: At enrollment, the 89 children exhibited severe immune defects. Antiretroviral therapy raised CD4+ T-lymphocyte counts significantly and decreased viral loads. In contrast, the in vitro immune parameters studied were not improved, except for plasma levels of sTNF-RII which decreased in parallel with the decrease in viral load. In addition, there was a trend towards increased skin test reactivity for the ritonavir-treated children. No differences were seen in the immune parameters whether the patients were treated with mono- or triple therapy. Results obtained after 120 weeks of therapy demonstrated that defective interleukin-12 production was not restored by long-term therapy.

Conclusions: After 6 months of therapy, with the exception of decreased sTNF-RII levels, and a trend towards increased skin test reactivity, restoration of several defective cellular immune responses did not occur despite significantly decreased viral loads and increased CD4+ T-lymphocyte counts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Anti-HIV Agents / therapeutic use*
  • Apoptosis
  • CD4 Lymphocyte Count
  • Child
  • Child, Preschool
  • Clinical Trials as Topic
  • Cytokines / biosynthesis
  • Cytokines / blood
  • Drug Therapy, Combination
  • HIV Infections / drug therapy*
  • HIV Infections / immunology*
  • HIV Protease Inhibitors / therapeutic use*
  • Humans
  • Immunity, Cellular
  • Indinavir / therapeutic use
  • Infant
  • Lymphocyte Activation
  • Reverse Transcriptase Inhibitors / therapeutic use*
  • Ritonavir / therapeutic use
  • T-Lymphocytes / immunology
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Viral Load

Substances

  • Anti-HIV Agents
  • Cytokines
  • HIV Protease Inhibitors
  • Reverse Transcriptase Inhibitors
  • Tumor Necrosis Factor-alpha
  • Indinavir
  • Ritonavir