Mice infected with Mycobacterium tuberculosis BCG were more resistant than normal mice to ectromelia virus infection. It is suggested that enhanced interferon production in peritoneal exudate cells and spleen cells of BCG-infected mice plays an important role in this resistance.

The mechanism of enhanced resistance of Mycobacterium bovis BCG-treated mice to ectromelia virus infection was investigated by determining the effect of splenectomy, antithymocyte. serum, and antimacrophage serum on resistance. It was greatly reduced by these treatments, not only in normal mice, but also in mice treated with live or heat-inactivated BCG. Production of circulating interferon by ectromelia virus and Newcastle disease virus was augmented in BCG-treated mice and was markedly depressed by splenectomy and antithymocyte and antimacrophage serum treatments in both BCG-treated and normal mice. Carbon clearance activity was activated in BCG-treated mice, but splenectomy did not influence phagocytic activity. These results suggest that augmented interferon production in the spleens of BCG-treated mice plays a major role in enhanced resistance. Other possible mechanisms are discussed. control mice was done as above except there was no excision of spleen.Cells. L-929 cells were cultivated in Eagle minimum essential medium supplemented with 10%o calf serum.Mouse embryo fibroblast cell cultures were prepared by trypsinization of 16-day-old DDN mouse embryos. The cells were cultivated with Eagle minimum essential medium-109o calf serum.Viruses. The Ishibashi strain of ectromelia virus was kindly supplied by Y. Ichihashi, . 1971. Role of macrophages and antibody in resistance of mice against yellow fever virus.

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