Peter H. Duesberg, Mike M.-C. Lai and Jan Maisel    Hämatol. Bluttransf. Vol 14

Virus Laboratory and Department of Molecular Biology, University of California, Berkeley, California 94720


The RNAs of several classes of avian and murine RNA tumor viruses were compared. The 60- 70S RNA complex of cloned nondefective avian sarcoma viruses contains only 30-40S RNA species of class a, which are larger than the 30-40S RNA species of class b found in avian transformation-defective or leukosis viruses. The RNA of a recombinant avian sarcoma virus, carrying a host range marker of a leukosis virus parent, also consists only of class a subunits. This implies that recombination among avian tumor viruses involves crossing-over rather than reassortment. The class a RNA subunits of nondefective avian sarcoma viruses and the class b RNAs of transformation-defective, leukosis viruses of the same subgroup and strain have very similar oligonucleotide-fingerprint patterns and are at least 60 % homologous if com pared by RNA-DNA hybridization. It is suggested that the class b RNA of leukosis viruses is a deletion of class a RNA from corresponding nondefective sarcoma viruses and that their structural relationship may be expressed as a= b + x. We assume, that x represents genetic information directly or indirectly involved in transformation of fibroblasts.
Passage at high multiplicity of cloned sarcoma viruses, containing only 30-40S RNA of class a, led to the appearance of 30-40S RNA of class bin progeny virus. Two replication-defective avian sarcoma viruses (Bryan RSV and MC 29) lack 30-40S RNA of class a. They probably contain distinct types of 30-40S RNA resembling class b RNA of leukosis viruses in size but differing in composition. The Kirsten murine sarcoma virus, which appears to be more defectice than Bryan RSV or MC 29, has a 30-40S RNA which is even smaller than of its leukosis helper virus. These observations suggest that a correlation exists between the size of the viral RNA species and defects in transformation-and(or replication genes of the corresponding viruses. The greater the extent of the defectiveness, the smaller is the size of the viral RNA. Possible mechanisms generating deletions in tumor virus RNA are discussed.