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It was recently reported that cells derived from some chick embryos are highly resistant to infection with Rous sarcoma virus (RSV) when challenged in vitro.' A virus was isolated from the resistant cells which induced resistance to RSV in chick embryo cells. Although the virus was named RIF, an acronym for "resistance inducing factor," it proved to be indistinguishable from the virus of visceral lymphomatosis (VLV) in its physicochemical, immunological, and biological characteristics. 1 2 It has been shown that four established strains of VLV can be detected in tissue culture by interference with RSV,l and we recently observed that avian myeloblastosis virus can also be detected in this way. The epidemiological behavior of RIF further supported its suggested relation to VLV. RIF, for example, was found to occur in highest frequency in the embryos of a chicken flock selected for a high incidence of neural and visceral lymphomatosis. The occurrence of RIF in embryos apparently normal in every respect indicates that congenital infection plays an important role in perpetuating the virus under natural conditions. A similar picture for VLV has been reported by Burmester' who found that VLV could be isolated from apparently healthy embryos. Recently we have isolated RIF from 22 of 33 cases of lymphomatosis occurring in the field in Northern California. Since RIF and VLV have given identical results in every characteristic which has been examined, RIF should be considered a California strain of VLV. The in vivo techniques which have been used to assay VLV are extremely cumbersome and time-consuming.4 By way of comparison the assay of RIF and various other VLV strains by interference with RSV is quick and efficient. The utility of the assay and the proximity of a heavily infected flock of chickens facilitated the present detailed investigation of the congenital transmission of RIF. The roles of male and female parents in congenital infection and particularly the relation of parental viremia and antibody titer to congenital infection were evaluated. The evidence to be presented shows that the parental flock was composed of birds with and without persistent RIF-viremia. Those with viremia had no detectable neutralizing antibody to RIF. Those without viremia had neutralizing antibody, and the titer of antibody remained relatively constant over a 10-month period. All the viremic hens transmitted infection through the egg to most of their progeny while only one of the nonviremic hens did so. Viremic roosters failed to transmit infection congenitally.

THE PATTERN OF CONGENITAL TRANSMISSION OF AN AVIAN LEUKOSIS VIRUS