Induction of apoptosis by herpes simplex virus-1 in neonatal, but not adult, neutrophils.
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.
Ennaciri
Jamila
J
Sainte-Justine Hospital Research Center, Faculty of Medicine, University of Montreal, Quebec, Canada.
Menezes
José
J
Proulx
François
F
Toledano
Baruch Joseph
BJ
D000328:Adult; D019138:Antibodies, Blocking / Q000494:pharmacology; D017209:Apoptosis; D053222:Fas Ligand Protein; D006561:Herpes Simplex / Q000276:immunology* / Q000473:pathology / Q000821:virology; D018259:Herpesvirus 1, Human; D006801:Humans; D007231:Infant, Newborn; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000821:virology*; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors / Q000378:metabolism; D019014:fas Receptor / Q000187:drug effects / Q000378:metabolism
D019138:Antibodies, Blocking; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D000079424:Tumor Necrosis Factor Inhibitors; D048069:Tumor Necrosis Factors; D019014:fas Receptor