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Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Department of Microbiology and Immunology, University of Melbourne, Victoria 3010, Australia

Correspondence
Margot Anders
emanders{at}unimelb.edu.au

Inactivated influenza A virus and fixed, virus-infected cells induce type 1 interferon (IFN-/) production in murine splenocytes. In this study, we have explored the nature of the virus–spleen cell interaction that leads to IFN-/ induction and the reason for the poor response to some virus strains. IFN-/ induction by horse serum-sensitive, but not -resistant, strains of influenza virus was inhibited in the presence of horse serum, indicating that binding of the virus to sialylated cell receptors is a necessary step in the induction process. Furthermore, influenza viruses A/PR/8/34 (H1N1) and A/WS/33 (H1N1), which were poor inducers of IFN-/ in spleen cells, were shown to have a more active neuraminidase than strains that induced higher IFN levels, and IFN-/ induction by A/PR/8/34 (H1N1) and A/WS/33 (H1N1) was restored in the presence of a neuraminidase inhibitor. Growth of virus in different cell types altered the level of IFN-/ induced in spleen cells by particular virus strains, suggesting that the nature of the carbohydrate moieties on the viral glycoproteins may also influence IFN-/ induction in this system. Consistent with this notion, treatment of egg-grown virus with periodate to oxidize viral carbohydrate greatly reduced its capacity for IFN-/ induction. Furthermore, induction of IFN-/ was inhibited in the presence of the saccharides yeast mannan and laminarin. Together these findings indicate: (i) a requirement for interaction of the virus with sialylated receptors on the IFN-producing cell; (ii) an influence of viral carbohydrate on the response; and (iii) possible involvement of a lectin-like receptor on the IFN-producing cell in the induction of IFN-/ or in regulation of this response.

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