Abstract
Rous-associated virus 7 (RAV-7) is a subgroup C avian leukosis virus which does not transform cells in vitro or carry an oncogene. When injected into 1-day-old hatched chicks, RAV-7 causes a low incidence of lymphoid leukosis after a latent period of several months. In contrast, infection of 10-day-old chicken embryos with RAV-7 leads to a disease syndrome characterized by stunting, obesity, atrophy of the bursa and the thymus, high triglyceride and cholesterol levels, reduced thyroxine levels, and increased insulin levels (Carter et al., Infect. Immun. 39:410-422, 1983; J.K. Carter and R.E. Smith, Infect. Immun. 40:795-805, 1983). Histopathological examination of tissues from affected chicks revealed an accumulation of lipid in the liver and an extensive infiltration of the thyroid and pancreas by lymphoblastoid cells. In the present investigation, the subgroup specificity of this syndrome was investigated. Other subgroup C avian leukosis viruses (transformation-defective B77, transformation-defective Prague C strain of Rous sarcoma virus, and RAV-49) caused stunting, infiltration of the thyroid and pancreas, increased liver weights, decreased thyroxine levels, and increased insulin levels, but they did not cause a uniform, profound increase in triglyceride and cholesterol levels. Avian leukosis viruses of subgroup A [myeloblastosis-associated virus 1 causing osteopetrosis [MAV-1(O)] and RAV-1], subgroup B [MAV-2(O), MAV-2 causing nephroblastoma [MAV-2(N)], and RAV-2], subgroup D (RAV-50), and subgroup F (ring-necked pheasant virus and RAV-61) did not cause a syndrome identical to that induced by RAV-7. All of the viruses examined induced some stunting and a reduction in thyroxine levels which correlated with the stunting. The two subgroup F viruses caused an infiltration of the thyroid which may have been secondary to severe lung involvement. We conclude that the RAV-7 syndrome is unique, particularly in the induction of a hyperlipidemia.