An in vitro model has been developed to study the replication of ectromelia virus in murine macrophages (M phi).
Infection of
mineral oil-elicited peritoneal M phi cultures with either the virulent (Moscow) or attenuated (Hampstead) strain of ectromelia virus led to productive
infections. The kinetics of virus synthesis was similar to those seen following
infection of murine fibroblasts. In contrast, peritoneal M phi s activated by
intraperitoneal injection of
Corynebacterium parvum vaccine were found to be totally refractory to
infection by the attenuated strain and significantly more resistant to the virulent strain of ectromelia virus. Administration of C. parvum doses as small as 7 micrograms were sufficient to induce
antiviral activity. M phi resistance became maximal at 5-9 days after C. parvum administration; however, M phi resistance was unstable during in vitro culture. Decay of
antiviral activity was detected within the first 24 hr of culture and complete virus susceptibility returned after 5 days in culture. Peritoneal exudate cells (PEC) from C. parvum-immunized mice could induce resistance in susceptible M phi cultures during overnight cocultivation. In addition, cell-free culture supernatants from C. parvum-immune PEC could also induce resistance in susceptible M phi cultures, suggesting that a soluble factor, induced by C. parvum immunization and possessing
interferon activity, may account for the intrinsic resistance to ectromelia virus by activated M phi s.