Genetic recombination of RSV has been studied, using ts mutations in both initiation and maintenance of transformation as markers. The progeny of a single cycle of mixed infection appears to contain no recombinants, but yields heterozygous particles or viral clumps. On subsequent cycles of infection some of these heterozygotes/clumps persist, but they also segregate recombinant viruses. Some of the markers in these recombinants show evidence of linkage and thus probably recombine by intramolecular exchanges. Studies of td ts mutants (the class most frequently isolated from stock virus) show that recombination between them occurs at a level sufficient to explain cooperative transformation by these viruses. Furthermors, this genetic recombination is probably a necessary prerequisite for cooperative transformation since complementation between the mutants is absent or inefficient. The simplest explanation for this apparent lack of complementation is that the td ts mutants are all derived by lesions in the same cistron.