Abstract

The influence of the endogenous virus ev 6 on congenital transmission of EV21, the infectious viral product encoded by locus ev 21, and the immune response to exogenous avian leukosis virus (ALV) infection was studied in rapid-feathering (RF) female progeny from four classes of slow-feathering (SF) (ev 21+ and RF (ev 21−) dams with and without ev 6. Apart from transmitting infectious EV21 and ev 6 to progeny, dam ev genotype did not influence the immune response or shedding of RPL-40. The endogenous virus envelope glycoprotein encoded by ev 6, however, completely restricted shedding and congenital transmission of infectious endogenous virus EV21, from SF dams. After 19 wk of exposure to ALV strain RPL-40 infected cage mates, only 11% of the congenitally infected female progeny mounted neutralizing antibodies against RPL-40, whereas 73% of their noncongenitally infected sisters seroconverted. More ev 6+ female progeny, however, were shedders of RPL-40 and developed tumors than ev 6− sisters. Among progeny from the four classes of dams, EV21 congenitally infected hens had the highest incidence (31%) of RPL-40-induced tumors.

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