Herpes simplex virus type 2 inhibition of Fas ligand expression.
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.
Sieg
S
S
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106-4943, USA.
Yildirim
Z
Z
Smith
D
D
Kayagaki
N
N
Yagita
H
H
Huang
Y
Y
Kaplan
D
D
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D002522:Chlorocebus aethiops; D053222:Fas Ligand Protein; D018259:Herpesvirus 1, Human / Q000378:metabolism; D018258:Herpesvirus 2, Human / Q000378:metabolism*; D006801:Humans; D019169:Jurkat Cells; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins