Tumors were induced in adult and newborn rabbits by inoculation of fibroma virus. Whereas tumors completely regressed in adult rabbits by 3 weeks after virus inoculation, newborn rabbits supported tumor growth for 3 to 4 weeks. In the latter case, some animals died at this time, others survived with a gradual regression of the tumors over an additional period of 5 to 6 weeks. Virus neutralization studies demonstrated antibodies to fibroma virus in the serum from both adult and newborn tumor-bearing rabbits. Newborn rabbits with progressively growing tumors failed to elicit a delayed cutaneous hypersensitivity reaction to fibroma antigens, whereas adult rabbits showed strong reactions as early as 7 days after tumor induction. Similarly, macrophage migration inhibition tests revealed that the lymphocytes from newborn rabbits with progressively growing tumors were only weakly reactive to fibroma antigens, as compared to lymphocytes from adult tumorbearing rabbits. In contrast, newborn rabbits that survived and regressed the tumors demonstrated strong cell-mediated immunity both by skin testing and migration inhibition. Virus growth studies in cell culture demonstrated that fibroma was unable to replicate in peritoneal macrophages from either newborn or adult rabbits. No differences were observed in growth of the virus in macrophages from tumor-bearing rabbits. The significance of these observations is discussed in respect of the possible role of cell-mediated immunity in fibroma tumor regression.

Peritoneal macrophages recovered from chickens 15 to 20 days after inoculation with fowlpox virus and showing a delayed hypersensitivity reaction against fowlpox antigens demonstrated an enhanced antimicrobial effect against fowlpox virus as well as unrelated viruses and bacteria. Inoculation of normal chicken macrophage cultures with fowlpox virus resulted in approximately a 200-fold increase in virus titer by 96 h, whereas the virus showed less than a fourfold increase in macrophage cultures from fowlpox-immune chickens. Similarly, the titer of Newcastle disease virus increased by more than 1 log in cultures of normal macrophages, whereas the titer decreased by approximately 1 log after infection of fowlpox-immune macrophages. Vaccinia, vesicular stomatitis, and herpes simplex viruses, which are not natural pathogens of chickens, failed to replicate in cultures of either normal or fowlpox-immune macrophages. By using Salmonella gallinarum , it was further demonstrated that the antimicrobial activity of fowlpox-immune macrophages encompassed not only nonspecific viruses but also bacteria. Infection of normal macrophages with Salmonella resulted in intracellular replication of the organism between 0 and 24 h as determined by microscope examination and viable bacteria counts. In contrast, cultures of fowlpox-immune macrophages failed to show an increase in intracellular organisms and showed a marked decrease in viable bacteria. In conclusion, these studies clearly showed that cellular immunity, previously demonstrated in mammalian species, develops in chickens after infection with fowlpox virus.