Specificity of avian leukosis virus-induced hyperlipidemia

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

Identification of two novel multiple recombinant avian leukosis viruses in two different lines of layer chicken

“…The strains of ALV-C include RAV-7, RAV-49, B77 and Pr RSV-C. Sandelini & Estola (1974) isolated ALV-C in Finnish breeding flocks and reported that the antibody against ALV-C was widespread in Finland at that time. In natural or experimental infection, RAV-7 and RAV-49 mainly cause stunting, obesity, hypothyroidism, hyperinsulinaemia, alterations in lipid metabolism, meningoencephalomyelitis and a low incidence of lymphoid leukosis , 1984Heidrich et al, 1987;Whalen et al, 1988). The severity of these isolates, however, appears to be strain dependent (Karakoz et al, 1980;Smith & Schmidt, 1982;Stepanets et al, 2003).…”

Defective rotavirus particle assembly in lovastatin-treated MA104 cells

“…As lipids are critical to the biology of enveloped viruses, some of these viruses modulate the host-cell lipid metabolism to their advantage, by up-or down-regulating their lipid synthesis [2,8,16,28]. However, recent reports have demonstrated the involvement of lipids in the cell biology of a non-enveloped, double-stranded RNA virus, the rotavirus, as well [3,5,6,13,33].…”

Localization of Avian Leukosis Virus Subgroup J in Naturally Infected Chickens by RNA In Situ Hybridization

“…25 Although the vast majority of the research on these retroviruses has focused on their oncogenic properties, several studies have focused on their nonneoplastic effects and pathogenesis in younger chickens. Viruses in ALV subgroups A, B, C, and D produced stunting in growing chickens associated with a lymphocytic thyroiditis and lowered circulating thyroxine levels, with the most severe effects associated with ALV subgroup C. 7,8 RAV-1—a subgroup A ALV—induced myocarditis, right-sided heart failure, and ascites syndrome in immature chickens and was associated with the formation of viral matrix inclusion bodies in cardiac myocytes. 15,16 An ALV produced by a lymphoid leukosis cell line also induced ascites when inoculated into immature chickens.…”