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Poly I:C‐Induced Anti‐Herpes Simplex Virus Type 1 Activity in Inflammatory Macrophages Is Mediated by Induction of Interferon‐β
Author(s) -
Pyo S.,
Gangemi J.D.,
Ghaffar A.,
Mayer E.P.
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.50.5.479
Subject(s) - herpes simplex virus , interferon , biology , autocrine signalling , antibody , virology , macrophage , virus , cytokine , immunology , microbiology and biotechnology , cell culture , in vitro , biochemistry , genetics
We examined the mechanism by which Polyriboinosinic:Polyribocytidylic acid (Poly l:C) augments resistance of thioglycolate‐elicited inflammatory macrophages to infection with herpes simplex virus type 1 (HSV‐1). We show that Poly l:C‐induced antiviral activity is completely abrogated by antibodies to interferon‐β (IFN‐β) 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 l:C contain IFN‐β but not IFN‐α. Taken together these data indicate that the antiviral effects of Poly l:C in inflammatory macrophages are mediated solely by IFN‐β, which acts in an autocrine manner to induce resistance to HSV‐1.