Smith E J, Fadly A M, Crittenden L B
USDA, Agricultural Research Service, East Lansing, Michigan 48823.
Poult Sci. 1990 Aug;69(8):1251-6. doi: 10.3382/ps.0691251.
The influence of the endogenous virus ev6 on congenital transmission of EV21, the infectious viral product encoded by locus ev21, 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) (ev21+ and RF (ev21-) dams with and without ev6. Apart from transmitting infectious EV21 and ev6 to progency, dam ev genotype did not influence the immune response or shedding of RPL-40. The endogenous virus envelope glycoprotein encoded by ev6, 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 ev6+ female progeny, however, were shedders of RPL-40 and developed tumors than ev6- sisters. Among progeny from the four classes of dams, EV21 congenitally infected hens had the highest incidence (31%) of RPL-40-induced tumors.
研究了内源性病毒ev6对禽病毒21（EV21）先天性传播、由基因座ev21编码的传染性病毒产物以及对外源性禽白血病病毒（ALV）感染的免疫反应的影响，这些研究对象是来自四类慢羽（SF）（携带和不携带ev6的ev21+和RF（ev21-）母禽）的快羽（RF）雌性后代。除了将传染性EV21和ev6传播给后代外，母禽的ev基因型并不影响RPL - 40的免疫反应或排毒情况。然而，由ev6编码的内源性病毒包膜糖蛋白完全限制了来自SF母禽的传染性内源性病毒EV21的排毒和先天性传播。在接触感染RPL - 40毒株的笼养同伴19周后，只有11%的先天性感染雌性后代产生了针对RPL - 40的中和抗体，而其未先天性感染的姐妹中有73%发生了血清转化。然而，与ev6-的姐妹相比，更多的ev6+雌性后代是RPL - 40的排毒者且发生了肿瘤。在四类母禽的后代中，先天性感染EV21的母鸡发生RPL - 40诱导肿瘤的发生率最高（31%）。
