Influence of thromboxane synthetase inhibitors on virus replication in human lung fibroblasts in vitro.
Selective modulation of cellular arachidonic acid metabolism with thromboxane synthetase inhibitors temporarily reduced the yield of viruses hosted by human lung fibroblasts in vitro. The results were similar for several viruses including type I herpes simplex virus, vaccinia, vesicular stomatitis virus, chikungunya virus, and Newcastle disease virus. Thromboxane synthetase inhibitors of different structural classes were effective and their effects were confined to cells that contain the thromboxane synthetase. Virus yields were unaltered by total inhibition of arachidonic acid oxidative metabolism or exogenous addition of prostaglandins. In contrast to most cytopathic agents, viruses destroyed host cells without stimulating prostaglandin synthesis unless interferon induction accompanied the infection in vitro. The results suggest that cellular arachidonic acid metabolism may contribute to the host defense response during virus infections.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D002478:Cells, Cultured; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D010088:Oxidoreductases / Q000037:antagonists & inhibitors*; D018139:Simplexvirus / Q000254:growth & development; D013329:Structure-Activity Relationship; D013928:Thromboxane A2 / Q000502:physiology; D013930:Thromboxane-A Synthase / Q000037:antagonists & inhibitors*; D014779:Virus Replication / Q000187:drug effects*
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D013928:Thromboxane A2; D010088:Oxidoreductases; D013930:Thromboxane-A Synthase; D007213:Indomethacin