Earlier studies showed that recombinant and naturally occurring subgroup A avian leukosis viruses (ALV) could be introduced into the chicken genome by injection of the virus into the yolk of unincubated fertile eggs and could re‐insert into the germline spontaneously (Crittenden & Salter, 1988; Crittenden et ah, 1989). The proportion of proviruses that were complete and produced infectious virus was considerably higher than found for the naturally occurring ALVE (ev) family of endogenous viral genes found in domestic chickens. These studies extend earlier observations on spontaneous insertion and show that congenital infection of inherited‐provirus‐free males can result in germline insertion at a high frequency in the progeny of about 50% of them, and that a small proportion of birds carrying artificially introduced proviruses produced progeny carrying new germline inserts at a high rate by migration of the provirus to new genomic locations. The evidence suggests that the most likely mechanism is the infection of primary germ cells at some time during development. Matings for several generations showed that genomic mobility of some inserts was stable suggesting that the location of insertion may have controlled the expression of the virus produced by the inserts at high titres at the appropriate time in development for germ‐cell infection. We suggest that we have recapitulated germline infection events, suggested by Frisby et al. (1979), that led to infection of the germline of the Red Jungle Fowl and spread of endogenous viral genes through the genome during early domestication. We also postulate that natural selection against endogenous viral genes that have high virus expression phenotypes may account for the fact that germline mobility is not now commonly observed for naturally occurring ALVE genes.
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Crittenden et al. (1998) studied this question.
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