Abstract
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 not HSV-1, to inhibit the activity and cell surface expression of Fas ligand, an important molecule involved in T-cell apoptosis and cell-mediated cytotoxicity. Cells infected with HSV-2 retained Fas ligand intracellularly instead of expressing it on the cell surface. Addition of anti-Fas antibodies markedly inhibited HSV-2 viral production, suggesting that the capacity of the virus to regulate Fas ligand expression, and thereby programmed cell death, may represent a powerful mechanism for the virus to enhance viral replication.
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