High Error Rates, Population Equilibrium, and Evolution of RNA Replication Systems

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Abstract
It was often observed in the initial studies on mutagenesis of RNA viruses that wild-type revertants arose and contaminated clonal mutant preparations. In addition, it was noted that the so called “wild-type” virus included significant proportions of mutant genomes. Granoff 1 , 2 identified several spontaneous plaque-type (small, turbid) mutants of Newcastle disease virus (NDV) which occurred at variable frequencies that occasionally reached 1.5 × 10−1. Pringle 3 characterized many ts mutants of vesicular stomatitis virus (VSV) Indiana serotype that had been induced by various mutagenic agents. The yield of revertant phenotypes in such preparations was quite high and variable. For one mutant it reached 0.19 (ratio of plaques of mutant and wild type plated at the restrictive temperature). For others, it was −3 revertants. One “subclone” derived from this mutant did not synthesize viral RNA in the infected cells, while another “subclone” of the same preparation did so normally. 4 Genetic instability was found with other VSV mutants. 5 , 6 In those studies the frequency of spontaneous ts phenotype in VSV was 1% and 2% with nonpermissive temperatures of 39.0 and 39.8°C, respectively. The early evidence of genetic variability of rhabdoviruses has been reviewed. 7 – 9

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