Abstract:
An investigation of the mechanism of resistance expressed by normal mouse macrophages against IHD vaccinia virus infection was conducted. Results from virus growth assays showed that vaccinia virus is incapable of multiplying in unstimulated mouse macrophages and instead is degraded by them. Studies concerning first stage uncoating of virus using sodium suramin as a host lysosome stabilizer indicated no change in viral liters and acid phosphatase particulate staining. This indicated that first stage uncoating of virus was not achieved due to lack of phagosome-lysome fusion in the presence of suramin. Electron micrograph studies revealed the presence of cytoplasmic cores, indicative of first stage uncoating, in both resistant and susceptible cells. Further studies concerning the second stage of uncoating indicated presence of degraded radioactive viral nucleotides in the supernatant of both mouse and rabbit peritoneal macrophages. Autoradiography studies of infected mouse and rabbit macrophages showed that no significant viral DNA synthesis occurred in mouse cells when compared to ravvit cells. This indicated that the block of the virus replicative cycle in mouse cells occurs early during the infection. Evidence obtained points to the suppression of viral DNA synthesis in normal mouse macrophages as a means of expressing innate immunity against vaccinia virus. One possible mechanism for the block early in the replicative cycle of vaccinia is the presence of interferon in mouse cells.
