title: Herpes simplex virus type 2 inhibition of Fas ligand expression.
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.
authors.affiliation: Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106-4943, USA.
authors.forename: S
authors.initials: S
authors.lastname: Sieg
authors.forename: Z
authors.initials: Z
authors.lastname: Yildirim
authors.forename: D
authors.initials: D
authors.lastname: Smith
authors.forename: N
authors.initials: N
authors.lastname: Kayagaki
authors.forename: H
authors.initials: H
authors.lastname: Yagita
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
authors.forename: D
authors.initials: D
authors.lastname: Kaplan
mesh_terms: 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
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins