Hens from a commercial source were selected because they were infected with lymphoid leukosis virus (LLV). LLV was detected in vaginal swabs from 17 viremic hens and from 27 of 44 hens that were not viremic. All hens that were positive on the vaginal swab test (VST) produced one or more eggs with virus in albumen or in embryos, whereas in comparable tests, virus was detected only in eggs from 5 of 17 hens that were negative on VST. Congenital transmission of LLV was erratic and neither the VST nor tests for virus in egg albumen prior to incubating eggs identified all hens that transmitted infection. For example, 14 hens negative on VST produced 50 eggs negative for virus in albumen and yet one of the embryos from these eggs was infected. Eggs from other hens had infectious virus in albumen and about half of the embryos from these were infected. Tests for virus in cloacal swabs from one-day-old chicks were as sensitive as tests on embryos for detecting congenital transmission. Titers of LLV in the meconium of congenitally infected chicks were as high as 10(7) infectious units per ml. The cloacal swab test should be a valuable adjunct to the VST and tests on egg albumen in programs designed to eradicate lymphoid leukosis from chickens.

SUMMARYLymphoid 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.

Three groups of pullets--those lacking endogenous viral (ev) genes, those carrying ev3, which codes for avian leukosis virus (ALV) group-specific (gs) antigen but not complete virus, and those carrying ev2, which codes for complete endogenous virus--were reared to maturity free of exogenous ALV infection or reared separately after inoculation at 1 day with ALV. The enzyme-linked immunosorbent assay (ELISA) was used to detect gs antigen in feather pulp, cloacal swabs, sera, white blood cells, and albumens from the pullets and in embryos, combs, and meconia from their progeny. These results were used to identify methods to distinguish between endogenous ALV expression and exogenous ALV infection. Although the frequency and levels of gs antigen detection were higher in most of the ALV-positive than in ev-positive ALV-negative materials, albumens and cloacal swabs had the lowest frequency of gs antigen detection in the ev-positive ALV-negative materials. These two materials had a further advantage in that detection of gs antigen in them has been shown to be highly correlated with congenital transmission. Further studies using ELISA absorbance values and titer to quantitate gs antigen showed that ev-positive ALV-negative albumens had much lower levels of gs antigen than ALV-positive albumens. The same criteria were not useful for distinguishing cloacal swabs of these two types. We conclude that in these lines, high levels of gs antigen in albumen is a sensitive and practical means of identifying dams congenitally transmitting ALV, because there is a very low frequency of "false positives" due to endogenous gs antigen in this material.

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Summary Two chicken genomic libraries were screened for the presence of poly(TG/AC) microsatellite tracts. The number of positive clones was low, confirming the low frequency of such micro‐satellites in the chicken genome relative to mammalian genomes. Polymorphism of 29 microsatellite tracts, comprising 11 from the library screening and 18 obtained from GenBank, was examined in the East Lansing and Compton reference families, in a resource population formed by a cross between a single White Rock broiler and inbred Leghorn females, and in a panel of birds from five layer stocks. Twenty microsatellites, primarily of the poly(TG/AC) type, were polymorphic in at least one of the populations. Thirteen of the microsatellites were polymorphic in the East Lansing reference family and 13 were also polymorphic in the resource population, confirming that the genetic distance between White Rock and White Leghorn is about as great as between Jungle fowl and White Leghorn. Only six microsatellites were polymorphic in the Compton reference family, formed by a cross between two White Leghorn strains. Twelve of the microsatellites were mapped in the East Lansing and/or Compton reference families. These were well dispersed among the various linkage groups and did not show any indications of terminal clustering.