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Title: RESPONSE OF WHITE LEGHORN CHICKENS OF VARIOUS GENETIC LINES TO INFECTION WITH AVIAN LEUKOSIS VIRUS SUBGROUP J

Author
item WILLIAMS, SUSAN - MICHIGAN STATE UNIVERSITY
item REED, WILLIE - MICHIGAN STATE UNIVERSITY
item Bacon, Larry
item Fadly, Aly

Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/30/2003
Publication Date: 1/1/2004
Citation: Williams, S.M., Reed, W.M., Bacon, L.D., Fadly, A.M. 2004. Response of white leghorn chickens of various genetic lines to infection with avian leukosis virus subgroup J. Avian Diseases. 48:61-67.

Interpretive Summary: Subgroup J avian leukosis virus (ALV-J) is an economically important virus infection that can cause cancerl-ike disease and other production problems primarily in meat-type chickens. Recent observations suggest that the virus can also infect egg-type chickens, but the influence of various genetic components on the response of these egg-type chickens to ALV-J infection is not known. Our data show that genetic differences among lines of egg-type (white leghorn) chickens, including the presence or absence of an endogenous genetic element termed endogenous virus 21 (EV21), may influence response of chickens to infection with ALV-J.This new information is significant and useful to scientists in academia and industry who are studying the epidemiology and control of this important virus infection of chickens.

Technical Abstract: Chickens from various white leghorn experimental lines were infected with strain ADOL-Hc1 of subgroup J avian leukosis virus (ALV-J) either as embryos or at 1 day of age. In experiment 1, chickens were tested for ALV-J induced viremia, antibody and packed cell volumes (PCV) at various ages. At 4 and 10 weeks of age, bursal tissues were also examined for ALV-induced pre-neoplastic lesions using the methyl green-pyronine (MGP) stain. In experiment 2, chickens harboring or lacking endogenous virus 21 (EV21) were inoculated with strain ADOL-Hc1 of ALV-J at hatch. All embryo-inoculated chickens used in experiment 1 tested positive for ALV-J and lacked antibody throughout the entire experiment and were considered viremic-tolerant, regardless of line of chickens. By 10 weeks of age, the incidence of ALV-J viremia in chickens inoculated with virus at hatch varied from 0% (line 0 chickens) to 97% (line 15I5); no influence of ALV-J infection was noted on PCV. Results from microscopic examination of MGP-stained bursal tissues suggest that ALV-J may induce typical ALV-induced transformation in bursal follicles of white leghorn chickens. Lymphoid leukosis and hemangiomas were the most common ALV-J induced tumors noted in chickens used in this study. In experiment 2, at 31 weeks of age, 54% of chickens harboring EV21 were viremic-tolerant, compared with 5% of chickens lacking EV21 following inoculation with ALV-J at hatch. The data indicate that genetic differences among lines of white leghorn chickens, including the presence or absence of EV21, may influence response of chickens to infection with ALV-J.