ROLE OF TREHALOSE DIMYCOLATE-INDUCED INTERFERON-ALPHA BETA IN THE RESTRICTION OF ENCEPHALOMYOCARDITIS VIRUS GROWTH IN-VIVO AND IN PERITONEAL MACROPHAGE CULTURES/

Preventive intraperitoneal trehalose dimycolate (TDM) treatment of mic e, inoculated with encephalomyocarditis (EMC) virus by the same route, caused restriction of virus growth in the peritoneum, which was corre lated to IFN production in peritoneal fluids prior to infection. Perit oneal macrophages from TDM-treated mice (TDM-PM) spontaneously secrete d IFN-alpha/beta in large amounts. By their supernatants, TDM-PM could transfer an antiviral state against EMC virus to permissive resident peritoneal macrophages from control mice. IFN-alpha/beta produced by T DM-PM was found to be involved in this transfer activity. TDM-PM also exerted a strong antiviral effect on EMC virus-infected L-929 cells, w hich increased with time and the macrophage-target cell ratio. This ac tivity also occurred by an IFN-alpha/beta-dependent mechanism. These d ata point to the role of IFN-alpha/beta production prior to EMC virus infection in the antiviral activities of TDM-PM and, more generally, i n the outcome of viral infection.