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A virus isolated from adult turkey tissue, when inoculated into 1- to 14-day-old chicks, Japanese quail, and turkey poults, produced reticuloendotheliosis. Homogenized liver and spleen cells containing virus as source inoculum within 21 days consistently caused 100% deaths of White Leghorn Dekalb 151 line chickens and progeny of White Rock roosters crossed with White Cornish hens. In contrast, the virus purified by differential centrifugation from plasma of infected chickens or tissue culture fluid rarely caused 100% deaths. The virus grown in quail-embryo fibroblast culture did not interfere with the Bryan strain of Rous sarcoma virus. Results with the RIF (resistance-inducing factor) and COFAL (complement fixation avian leukosis) tests were negative when the antigen contained only the virus. When inoculated on chick-embryo chorioallantoic membrane, the virus produced large, solitary, pocklike lesions. Embryos were discolored green but were usually alive 10 days after virus inoculation of either the chorioallantoic membrane or the allantoic sac. The virus was not neutralized by antisera to B, H, or SR strain of Rous sarcoma or RPL12 strain of lymphomatosis or BAI-A strain of myeloblastosis leukosis viruses. Specific antisera against the present virus did not neutralize the B strain of RSV, although antisera prepared against the B strain of RSV neutralized the virus. The virus, designated RE (strain T), is not considered related to previously described avian leukosis viruses. The RE virus has the following characteristics: 1) It produces rapid proliferation of the reticuloendothelial cells with death following a peracute-to-acute course in young Japanese quail, turkeys, and chickens; 2) it appears to be antigenically unrelated to several of the known avian leukosis viruses; 3) if is RIF and COFAL negative,-4) it replicates in either quail or chicken fibroblasts in tissue culture; 5) its particles differ morphologically from the previously described avian leukosis viruses; and 6) it is stable at—70 C, but the biological activity is destroyed by heating at 56 C for 30 minutes or by exposure to ether.
Theilen et al. (Thu,) studied this question.