Submitted to: Congress on In Vitro Biology
Publication Type: Abstract Only
Publication Acceptance Date: January 30, 2006
Publication Date: March 1, 2006
Citation: Goodman, C.L., Mcintosh, A.H., Stanley, D.W. 2006. Eicosanoids influence insect cell-viral interactions [abstract]. Congress on In Vitro Biology. 42:2A. Technical Abstract: Eicosanoids are oxygenated, enzymatic metabolites of arachidonic acid, including prostaglandins and an array of lipoxygenase products. These signaling compounds are important in vertebrate and invertebrate biology. In insect immunity, eicosanoids mediate and coordinate specific cellular actions responsible for clearing infections (including bacterial, fungal, protozoan and parasitic) from circulation. The signaling mechanisms responsible for the widely varying insect resistance to viruses, however, remain unknown. In this poster we present an overview of eicosanoid structures and report on experiments designed to test our hypothesis that eicosanoids also exert important actions in the interactions between insect cells and viruses. To test our hypothesis, we used two cells lines, one non-permissive to viral infection (HzAM1, a pupal ovarian line from Helicoverpa zea) and one permissive (HvAM1, a pupal ovarian line from Heliothis virescens). Treating the HzAM1 line with inhibitors of eicosanoid biosynthesis, then challenging the cultures with the AcMNPV baculovirus, resulted in significantly increased proportions of cells producing virus and higher overall extracellular virus concentrations. We infer that eicosanoids influence one or more cellular mechanism(s) of viral resistance. Similar experiments with the permissive HvAM1 line resulted in significantly decreased proportions of cells producing virus early in the infection process although this reduction was overcome later in the infection. Inhibitor-treated cells also produced significantly reduced levels of extracellular virus. Our data on a permissive and a non-permissive cell line indicate that eicosanoids influence cellular events required for either permitting or not permitting viral entry and replication.