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CD95 expression and apoptosis during pediatric HIV infection: early upregulation of CD95 expression

T W McCloskey1, N Oyaizu, S Bakshi

  • 1Department of Pediatrics, North Shore University Hospital-New York University School of Medicine, Manhasset 11030, USA.

Insights

Pediatric HIV infection accelerates immune decline. Early CD95 antigen expression on T cells in infants with pediatric HIV may precede apoptosis, impacting disease progression.

Area of Science:

  • Immunology
  • Pediatric Infectious Diseases
  • Cell Biology

Background:

  • Pediatric HIV infection leads to rapid CD4 T lymphocyte decline and immune dysfunction.
  • Apoptosis, potentially via CD95 antigen, is a proposed mechanism for T cell loss in HIV.
  • Disease progression is generally faster in children than in adults with HIV.

Purpose of the Study:

  • To investigate CD95 expression and apoptosis in pediatric HIV infection.
  • To correlate CD95 expression and apoptosis with immunologic categories in HIV-infected children.
  • To determine the timing of CD95 upregulation in relation to apoptosis in infants with perinatally acquired HIV.

Main Methods:

  • Analysis of peripheral blood lymphocytes from HIV-infected children across CDC immunologic categories.
  • Flow cytometry to quantify CD95 expression on CD4 and CD8 T cells.
  • Assessment of lymphocyte apoptosis rates.

Main Results:

  • Increased percentages of CD95-expressing CD4/CD8 T cells and apoptotic lymphocytes were observed in HIV-infected children.
  • Higher CD95 expression and apoptosis rates were found in immunologic Category III compared to Category I.
  • Elevated CD95 expression was detected as early as 3 months of age, preceding increased apoptosis.

Conclusions:

  • HIV-infected infants show early CD95 upregulation, even before significant apoptosis.
  • This early CD95 expression aberration may play a critical role in the pathogenesis of perinatally acquired HIV disease.
  • Findings suggest CD95 may be an early indicator of immune dysregulation in pediatric HIV.

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