Abstract
Mammalian (LLC-MK2) cell monolayers pretreated with either chromium or manganese particles depressed viral induction of IFN by approximately 50% but the presence of metal particles did not prevent exogenous IFN from conferring antiviral cellular resistance. Manganese particles were more detrimental to viral IFN induction than chromium particles in that almost tenfold less of the former achieved a comparable magnitude of IFN inhibition. Although rates of influenza virus multiplication in either chromium or manganese-treated and control cell cultures were similar, virus attained a level of growth almost twofold higher in metal-treated cells than in controls. This was related to suppression of viral IFN induction by metal particles. Neuraminidase treatment of cell surface salioglycoproteins or pretreatment of chromium or manganese particles with sialic acid abrogated the adverse activity of metal particles on viral IFN induction. These findings suggest that the receptivity and interaction of cell membrane-bound sialic acid residues with metal particles are involved in the altered cellular protective response described.
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