Role of contact and genetic transmission of endogenous virus-21 in the susceptibility of chickens to avian leukosis virus infection and tumors.

The role of contact and genetic transmission of endogenous virus-21 (EV21) on response of chickens to avian leukosis virus (ALV) infection and tumors was studied. F1 progeny of a cross between RPRL late-feathering (LF) line EV21+ males and RPRL early feathering (EF) line 15B1 females harboring or lacking EV21 were used. The EF chicks lacking EV21 were inoculated with a field strain of subgroup A ALV at hatch and contact exposed to LF, EV21+ hatchmates for various time intervals. In a second experiment, EV21 contact-exposed and unexposed EF chicks as well as LF, EV21+ hatchmates were inoculated with ALV at various ages. Chickens were tested for ALV-induced viremia and antibody and were observed for tumors until 24 wk of age. Antibody to EV21 in EF chickens contact-exposed to LF, EV21+ hatchmates varied from 10 to 65%, and was detected by 10 wk of age. By 24 wk of age, ALV-induced viremia and tumors in EF chickens varied from 5 to 30%, and from 15 to 32%, respectively, regardless of exposure to EV21. The incidence of ALV-induced tumors was significantly higher in LF chickens genetically infected with EV21 than in EV21 contact-exposed or unexposed EF chickens, but only in chickens inoculated with ALV at hatch. The data suggest that contact infection with EV21 has no influence on ALV infection and tumors. The data also suggest that genetic transmission of EV21 may increase susceptibility of chickens to ALV infection and tumors following infection with ALV at hatch, but not at 4 wk of age or older.