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Eight groups of 1-day-old or 8-week-old chickens were exposed by contact to lymphoid leukosis virus (LLV) infection. Five groups of about 60 spf chickens were used. Three groups of the same size were progeny from LLV vaccinated hens. Five groups were housed in one chicken house in close contact with a large number of immunologically tolerant chickens (virus "spreaders"). On two occasions infectious LLV was recovered from air/dust samples collected in this house. In the second house a small number of congenitally infected birds generated a mild degree of LLV exposure. It was demonstrated that infection by contact may lead to lymphoma formation and congenital virus transmission. The incidence of virus infection and LL mortality in the groups of birds exposed at 8 weeks of age were significantly lower than in chickens exposed at 1 day of age. In addition, about 100-fold differences in numbers of LLV-associated white blood cells were observed between both age groups. These results indicate that in addition to resistance to tumour formation, resistance to LLV infection develops in the chicken with increasing age. Maternal antibodies, present in three groups exposed at 1 day of age, reduced the rate of infection and the incidence of LL.

SUMMARYViraemia and neutralising antibodies were determined in chickens of six age-groups following inoculation with leukosis virus of subgroups A and B at the age of 1 day, and 2, 4, 6, 8 and 10 weeks respectively. The birds were kept in a filtered air positive pressure (FAPP) house. A seventh agegroup, accommodated in a separate FAPP-house, was used as an untreated control.

Six age groups of specified pathogen free White Leghorn chickens housed in the same filtered air, positive pressure building, were inoculated at 1 day, 2, 4, 6, 8 and 10 weeks of age respectively, with a mixture of leukosis viruses of subgroups A and B. Birds which died during the experiment were examined for gross and microscopical lesions. The incidence of lymphoid leukosis (LL) in the various groups was inversely proportional to the age of first virus exposure, Le., mortality was 62.5% in the group inoculated at 1-day-old and decreased to zero in the group inoculated at 10 weeks of age. In the age group inoculated at 8 weeks, only one chicken succumbed to the disease. Congenital transmission of leukosis virus (LV) was detected only in chickens inoculated immediately after hatching or at 2 weeks of age. In the latter group, all leukosis virus positive embryos were derived from one hen only. A seventh age group, housed in a separate filtered air, positive pressure building, served as uninoculated controls. Challenge infection was performed on the same day with chickens of all groups at ages varying from 59 to 71 weeks. Testing of pooled embryo extracts collected between 1 and 15 weeks post challenge did not change the virus shedding pattern. Even the chickens of the control group which were challenged (for the first time) at 71 weeks of age remained negative for congenital transmission. The results of this experiment show that the chickens inoculated with LV at 4 weeks of age or older had a low incidence of LL (decreasing to zero when the chickens were inoculated at 10 weeks of age) but did not congenitally shed virus.