Studies on genetic and vaccination-induced resistance of chickens to lymphoid tumor transplants. 1. Marek's disease tumor transplant (JMV)

• Published in: Avian diseases Vol. 20; no. 2; p. 268
• Main Authors: Spencer, J L, Gavora, J S, Hare, W C, Grunder, A A, Robertson, A, Speckmann, G W
• Format: Journal Article
• Language: English
• Published: United States 01.04.1976
• Subjects: Animals; Chickens; Female; Herpesviridae - immunology; Male; Marek Disease - genetics; Marek Disease - immunology; Marek Disease - pathology; Mitosis; Neoplasm Transplantation; Selection, Genetic; Sex Chromosomes; Transplantation, Homologous; Vaccination - veterinary; Viral Vaccines; Wings, Animal - pathology
• ISSN: 0005-2086
• DOI: 10.2307/1589265

Six strains and 4 inbred lines of chickens that differed in susceptibility to Marek's disease (MD) were inoculated in the wing web with JMV when 5 weeks old. Wing web tumors (WWT) developed in all strains and lines inoculated with low-passage JMV (JMV-L) but were largest in Cornell Strain S (highly susceptible to MD). Of 3 strains inoculated with high-passage JMV (JMV-H), only Strain S had appreciable WWT development. Seventy-five percent of the unvaccinated S strain chickens challenged with JMV-L or JMV-H died during the experiments, and approximately half of this mortality occurred during the second week postinoculation. Inbred Line GC ranked next in susceptibility to Strain S and was more susceptible than other lines and strains, including the strain from which it originated. Vaccination with turkey herpesvirus one week before challenge protected against mortality and suppressed WWT development. The effect on WWT development was less, however, in Strains S and NH than in other strains. The transplantability of the tumor was investigated with the use of sex chromosomes as cell markers. Five to 7 days postinoculation of male Strain S chicks with JMV-L or JMV-H, most cells in metaphase from wing web or visceral tumors were of female origin. By 56 days, only male cells were found in visceral tumors. The interpretation was that early lesions were due to tumor transplantation and later lesions were induced by virus.