Abstract

Avian RNA tumor viruses undergo recombination for host range, transformation and reverse transcriptase markers (Vogt 1971; Kawai and Hanafusa 1972; Weiss et al. 1973; Wyke 1973; Mason et al. 1974). In considering possible mechanisms of this recombination, two factors must be taken into account: (1) recombinants occur at a high frequency, and (2) the viral genome, a 60–70S single-stranded RNA, consists of several 30–40S pieces. These two factors suggest an analogy to the influenza viruses, which have a segmented genome and also show high frequency recombination resulting from the reassortment of markers situated on different genome segments. Similarly, avian RNA tumor viruses could recombine by exchanging 30–40S RNA pieces with different genetic markers. However, preliminary experiments did not support the hypothesis of reassortment between avian tumor viruses for recombination and suggested that molecular crossing-over might occur (Duesberg and Vogt 1973a; Vogt and Duesberg 1973). In the present communication we will...

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