The endogenous viruses of chickens are closely related to the exogenous avian leukosis viruses (ALV) yet as a group differ from these viruses in their host range, growth rate, and oncogenicity. The present study was undertaken to determine the patterns of relationship among the genomes of endogenous and exogenous ALVs. Complete or partial T1 oligonucleotide maps were prepared from the genomes of endogenous viruses that reside at eight distinct loci in chickens. Selected endogenous viruses and recombinants of endogenous or endogenous and exogenous viruses were characterized for host range and growth rate. From these data we could infer the following: (1) Endogenous viruses form a distinct lineage of ALVs with the most distinctive differences occurring in the portion of env that encodes host range and the U3 portion of the long terminal repeat; (2) The U3 sequences of endogenous ALVs determine the low growth rates of these viruses; and (3) Endogenous ALVs have distinctive oligonucleotide markers that allow them to be subclassified into distinct lineages. Our results suggest that endogenous viruses are derived from one another and not from exogenous field strains of ALV. This phenomenon may be related to the unique env encoded host range of endogenous ALVs, their unique U3 encoded growth rates, or perhaps their unique access, as residents of germ line DNA, to germ line cells.
|Original language||English (US)|
|Number of pages||22|
|State||Published - Apr 15 1983|
Bibliographical noteFunding Information:
We thank L. Crittenden and H. Hanafusa for providing some of the cells and viruses used in this study, and M. Champion and 0. Turetsky for skilled teeh-nical assistance. This work was supported by Grants CA 17659 (to J.C.) and CA 23806 and P30 CA 127708 (to H.R.) from the National Cancer Institute, and a grant from the Leukemia Association of America to P.N.T. J.M.C. is a recipient of a Faculty Research Award from the American Cancer Society; P.N.T. was a postdoctoral fellow of the National Cancer Institute; and K.F.C. was supported in part by Grant GM 07310 from the National Institutes of Health.