Abstract
Lymphoid leukosis is induced by exogenous retroviruses (LLV) that replicate via a DNA intermediate that is integrated into host somatic cell DNA. Variation in endogenous LLV expression is largely controlled by location of DNA proviruses integrated in the host germ-line and inherited as Mendelian genes. Present evidence suggests that endogenous viral genes (ev loci) arose from germ-line integration of exogenous LLVs and that those integrated ev loci expressing high levels of virus are at a selective disadvantage. Exogenous LLV infection leads not only to development of LL in some chickens but also to reduced productivity of layers. Results of preliminary experiments suggest that variation in ev locus expression influences non-oncogenic pathology and immune response after infection with an LLV known to be structurally related to ev loci. The effect of these loci on response to infection by unrelated micro organisms and on productivity should now be studied to determine whether the breeder should be concerned with these genes.
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