Poly I:C-induced anti-herpes simplex virus type 1 activity in inflammatory macrophages is mediated by induction of interferon-beta.
We examined the mechanism by which Polyriboinosinic:Polyribocytidylic acid (Poly I:C) augments resistance of thioglycolate-elicited inflammatory macrophages to infection with herpes simplex virus type 1 (HSV-1). We show that Poly I:C-induced antiviral activity is completely abrogated by antibodies to interferon-beta (IFN-beta) whereas antibodies to other interferons or to other cytokines have no effect. Furthermore, treatment of inflammatory macrophages with exogenous IFN renders them resistant to HSV-1, whereas treatment with other cytokines does not. In addition, we demonstrate that supernatants from macrophages treated with Poly I:C contain IFN-beta but not IFN-alpha. Taken together these data indicate that the antiviral effects of Poly I:C in inflammatory macrophages are mediated solely by IFN-beta, which acts in an autocrine manner to induce resistance to HSV-1.
Pyo
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Department of Microbiology and Immunology, University of South Carolina School of Medicine, Columbia 29208.
Gangemi
J D
JD
Ghaffar
A
A
Mayer
E P
EP
D000818:Animals; D006561:Herpes Simplex / Q000276:immunology*; D007113:Immunity, Innate / Q000276:immunology; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000378:metabolism / Q000502:physiology*; D008262:Macrophage Activation / Q000187:drug effects* / Q000276:immunology / Q000502:physiology; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011070:Poly I-C / Q000494:pharmacology*; D018139:Simplexvirus / Q000276:immunology* / Q000302:isolation & purification
D007371:Interferon-gamma; D011070:Poly I-C