Induction of apoptosis by herpes simplex virus-1 in neonatal, but not adult, neutrophils

Pediatr Res. 2006 Jan;59(1):7-12. doi: 10.1203/01.pdr.0000191816.57544.b4. Epub 2005 Dec 2.


We report a study on the effect of herpes simplex virus 1 (HSV-1) infection on apoptosis of neutrophils from both adults and neonates and present evidence showing that HSV-1 enhances apoptosis in neonatal, but not adult, neutrophils. HSV-1 enhanced the expression of both Fas and Fas ligand on the surface of neonatal neutrophils. Treatments with anti-Fas antibody and a Fas ligand inhibitor significantly reduced the induction of apoptosis by HSV-1. Using an ELISA assay, it was found that HSV-1 infection also leads to increased release of soluble FasL from HSV-1-infected neonatal neutrophils. Increased neonatal neutrophil apoptosis following HSV-1 infection may represent an important mechanism by which HSV-1 may diminish the antiviral response of neonatal neutrophils and might explain, at least in part, the severity of infections that are caused in newborns by this herpesvirus.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Blocking / pharmacology
  • Apoptosis*
  • Fas Ligand Protein
  • Herpes Simplex / immunology*
  • Herpes Simplex / pathology
  • Herpes Simplex / virology
  • Herpesvirus 1, Human*
  • Humans
  • Infant, Newborn
  • Membrane Glycoproteins / antagonists & inhibitors
  • Membrane Glycoproteins / metabolism
  • Neutrophils / immunology
  • Neutrophils / virology*
  • Tumor Necrosis Factor Inhibitors
  • Tumor Necrosis Factors / metabolism
  • fas Receptor / drug effects
  • fas Receptor / metabolism


  • Antibodies, Blocking
  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • Tumor Necrosis Factor Inhibitors
  • Tumor Necrosis Factors
  • fas Receptor