Abstract
Abstract Temperature-sensitive (ts) mutants of fowl plague virus (FU 67 and ts 7/36) have been isolated. They can be rescued to wild type by double infection with all standard ts mutants having single ts defects in any of the eight RNA segments. Rescue of FU 67 to wild type was not possible when ts mutants having simultaneous mutations in one of the RNA segments coding for the P proteins, the haemagglutinin, and nonstructural protein genes were used. After rescue with various prototype influenza A strains different RNA segments of FU 67 were replaced, depending on the strain used for rescue. The results are compatible with the idea that in FU 67 and ts 7 36 the ts phenotype is caused by the synergism of mutations in several RNA segments, each of which by itself is not sufficient to exhibit the ts phenotype.
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