AVIAN ACUTE-LEUKEMIA VIRUS MC29 - CONSERVED AND VARIABLE RNA SEQUENCES AND RECOMBINATION WITH HELPER VIRUS

The RNAs and proteins of five laboratory strains of defective avian acute leukemia virus MC29, differing in passage history and in some cases in their helper viruses and oncogenic spectra, were investigated for genetic variation. Earlier work based on homology with nondefective viruses of the avian tumor virus group has distinguished in 5.7-kb (kilobase) MC29 RNA a 5′ group-specific section, an internal MC29-specific section, and a 3′ group-specific section, and has determined that 5′ and internal sections together are translated into a nonstructural, gag gene-related 110K (kilodaltons) protein. The RNAs of the five MC29 strains analyzed here shared 20 conserved T1-oligonucleotides and differed in specific sets selected from 10 variable oligonucleotides. Since some, but not all, variable and some conserved MC29-oligonucleotides were shared with helper viruses, and since the 5′ cap-oligonucleotides of MC29 RNA rescued from the same nonproducer cell varied with that of the helper virus RNA, it is concluded that genetic variation of MC29 includes recombination with helper virus. Oligonucleotide maps of the five MC29 RNAs located 8 variable oligonucleotides in their 3′ group-specific sections, only conserved oligonucleotides in their internal-specific section, and mostly conserved oligonucleotides in their 5′ group-specific section (except for variable 5′ cap-oligonucleotides and the lack of an internal oligonucleotide in one strain). The 110K proteins of the MC29 strains were electrophoretically indistinguishable, which is in accord with the conserved nature of their templates. The ratio of MC29 RNA to helper virus RNA in virions was found to reflect, by a constant, the ratio of 110K MC29 to helper viral proteins in transformed cells. MC29 RNA is proposed to consist of two genetic units: one made of the highly conserved 5′ and internal-specific RNA sections, which codes for the 110K protein and appears to serve a primary function in oncogenicity; the other made of the variable 3′ group-specific RNA sections which may affect oncogenicity indirectly. © 1979.