|Pandiri, A - NORTH CAROLINA STATE UNIV|
|Gimeno, I - NORTH CAROLINA STATE UNIV|
|Reed, W - PURDUE UNIVERSITY|
|Fitzgerald, S - MICHIGAN STATE UNIVERSITY|
Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 15, 2008
Publication Date: March 1, 2009
Citation: Pandiri, A.R., Gimeno, I.M., Reed, W.M., Fitzgerald, S.D., Fadly, A.M. 2009. Subgroup J Avian Leukosis Virus-Induced Histiocytic Sarcomatosis Occurs Only in Persistently Viremic, but Not Immunotolerized Meat-type Chickens. Veterinary Pathology. 46(2):282-287. Interpretive Summary: Avian leukosis virus (ALV) is an economically important virus infection that can cause cancer like disease and other production problems in chickens. Previous observations suggest that a subgroup of ALV (ALV-J) may be involved in induction of cancerous lesions termed histiocytic sarcomatosis (HS) in meat-type chickens. These lesions have been detected in and caused condemnations of affected broiler chickens at processing plants. The conditions that allow the development of HS are poorly understood. We evaluated the influence of strain and dose of virus and age at infection on the development of HS in meat-type chickens. Our data show that HS was detected only in chickens that harbored virus for extended period of time following infection at hatch. This information is significant and useful to scientists who are studying the basic principals of tumor formation by this virus; the information should also be useful to industry scientists who are interested in minimizing the incidence of HS in their flocks.
Technical Abstract: Histiocytic proliferative lesions are sporadically reported in mammalian and avian species but the etiology and pathogenesis is not clear in most cases. However, in meat-type chickens, subgroup J avian leukosis virus (ALV J)-induced histiocytic sarcomatosis (HS) has been reported at a low incidence (1.1 – 8 %). The pathogenesis of HS is poorly understood. The effect of ALV J strain and dose, and age at infection on the development of HS was evaluated, retrospectively, in a study involving 174 meat-type chickens. Also, the effect of genetic line on the incidence of HS was evaluated in another experiment involving 75 meat-type chickens and 100 ADOL Line 0 chickens. HS was consistently observed in spleen along with frequent involvement of liver and kidney. The histiocytic nodules appeared to arise from the splenic ellipsoids and red pulp. Microscopically, the neoplastic histiocytes had polygonal to spindloid morphology and exhibited moderate anisocytosis and anisokaryosis. The neoplastic cells were diffusely positive for ChL5, CD45 and MHC class II. In addition, the gp85 viral antigen expression within HS was very low compared to other ALV J induced tumors. Results indicated that only persistently viremic meat-type chickens, but not ADOL line 0 chickens, inoculated at hatch develop HS with no effect of viral strain and/or dose. Unlike other ALV J induced tumors, HS was noted only in persistently viremic, but not immunotolerized meat-type chickens, suggesting possible different mechanisms of oncogenesis.