Experiments were conducted to establish whether B-haplotype genes that determine resistance to RSV-induced tumors would also influence resistance to Marek's disease and lymphoid leukosis. Matings of line 6(3) x 15(1) F3 or F4 breeders segregating for the Ea-B locus antigens that are markers for B2 and B5 haplotypes of the B major histocompatibility complex were made to produce B2B2, B2B5, and B5B5 chicks. The chicks were infected with a standard inoculum of one of the three tumor viruses in separate experiments. The B2 haplotype from 6(3) conveyed greater resistance to tumors induced by all three viruses than the B5 from 15(1) chickens. This finding suggests that some gene(s) in the B-haplotype may determine a general ability to resist tumor formation or cause tumor regression.

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Of chickens either spontaneously producing or exogenously infected in ovo with Rous-associated virus, type O (RAV-O), an endogenous virus of the chicken, only 1 died with lymphoid leukosis (LL), the most common neoplasm associated with the leukosis-sarcoma virus group. Because the chickens were not kept in strict isolation, it could not be assumed that the one LL was induced by RAV-O. In contrast, RAV-1-infected chickens from the same lines had a high incidence of LL and other neoplasms. Over 800 chickens of several inbred lines were maintained in plastic isolators free of exogenous avian leukosis-sarcoma virus infection for from 500 to nearly 1,000 days of age. No LL was observed, even though some lines are known to produce RAV-O spontaneously or to express inherited gs antigen. Three neoplasms of unknown etiology were observed, but none generally associated with leukosis virus infection. We concluded that avian endogenous virus expression had little, if any, oncogenic potential, and that exogenous avian leukosis viruses were responsible for most naturally occurring neoplasms.

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