Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are common human
pathogens, In this report we demonstrate the capacity of HSV-2, but no
t HSV-1, to inhibit the activity and cell surface expression of Fas li
gand, an important molecule involved in T-cell apoptosis and cell-medi
ated cytotoxicity. Cells infected with HSV-2 retained Fas ligand intra
cellularly instead of expressing it on the cell surface. Addition of a
nti-Fas antibodies markedly inhibited HSV-2 viral production, suggesti
ng that the capacity of the virus to regulate Fas ligand expression, a
nd thereby programmed cell death, may represent a powerful mechanism f
or the virus to enhance viral replication.