%0 Journal Article %A Miller, Joanna L. %A Anders, E. Margot %T Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells %D 2003 %J Journal of General Virology, %V 84 %N 1 %P 193-202 %@ 1465-2099 %R https://doi.org/10.1099/vir.0.18590-0 %I Microbiology Society, %X Inactivated influenza A virus and fixed, virus-infected cells induce type 1 interferon (IFN-α/β) production in murine splenocytes. In this study, we have explored the nature of the virus–spleen cell interaction that leads to IFN-α/β induction and the reason for the poor response to some virus strains. IFN-α/β 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-α/β in spleen cells, were shown to have a more active neuraminidase than strains that induced higher IFN levels, and IFN-α/β 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-α/β induced in spleen cells by particular virus strains, suggesting that the nature of the carbohydrate moieties on the viral glycoproteins may also influence IFN-α/β 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-α/β induction. Furthermore, induction of IFN-α/β 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-α/β or in regulation of this response. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.18590-0