Infection of 10-day chicken embryos with an avian leukosis virus, RAV-7, resulted in hypothyroidism within 3 weeks posthatching. Histological examination of the thyroids from infected chickens showed an extensive infiltration of lymphoblastoid cells by 7 days posthatching. Areas resembling germinal centers were present in the thyroids of infected chickens by 3 weeks posthatching. Examination of circulating thyroid and pancreas hormones showed a significant reduction in T3 and T4 levels and a trend toward higher insulin levels after 16 days posthatching. T4 supplementation of RAV-7-infected chickens alleviated some aspects of the disease syndrome but did not abrogate all symptoms. Marked involution of both bursa and thymus glands was noted. RAV-7 had an RNA genome of 8.2 kilobases and a polypeptide composition characteristic of an avian leukosis virus. The hypothyroidism followed a dose response to RAV-7 infection. Avian retroviruses have long been used to provide model systems for tumor formation. Induction of tumors in chickens by these viruses is either an acute response induced by viruses which carry their own oncogene, such as sarcoma viruses or defective leukemia viruses, or a chronic response induced by replication-competent viruses which carry no detectable oncogene (14). The latter group of viruses, the avian leukosis viruses, induce frankly neoplastic growths, such as B-cell lymphomas (4), proliferative disorders, such as osteopetrosis (30), and chronic degenerative diseases, such as anemia (25) and immunosuppression (34). Recent attention has been focused on the chronic debilitative diseases, since they may represent hitherto unrecognized consequences of retrovirus infection and provide model systems for diseases of humans (35). Chronic debilitation and stunting in animals can be the result of metabolic or endocrine

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