Our study explored the forces shaping the evolutionary history of class II aPMV-1 using available full genome sequences. We demonstrated that genotype affiliations based on individual genes and concatenated full length genomes of class II aPMV-1 were not consistent. This may account for discrepancies reported for genotype groupings that are based on partial or complete sequences of a single gene [13, 18, 43] . Topological incongruence among the gene trees reflects different evolutionary histories of each gene [44] ; recombination is the most plausible explanation for this. The role of recombination in the evolution of aPMV-1, and negative sense RNA viruses in general, has been debated. For example, Sakaguchi et al. [30] and Toyoda et al, [31] reported consistent topological placement of different NDV strains in both F and HN gene trees. Seal et al. [45] also reported that there was no evidence of recombination among NDV M gene sequences. Although recombination is more common in positive-sense RNA viruses and can be explained by several genetic mechanisms [46] , there is increasing evidence of homologous recombination in several non-segmented negative-sense RNA viruses [32, 47, 48, 49, 50] . Our approach differs from those used in previous studies of aPMV-1 evolution because we evaluated full genome sequences and tested individual recombinant regions with phylogeny-based incongruence tests. Thus, we show that all class II aPMV-1 genes have evidence of recombination breakpoints, that multiple recombination events are discernable in some isolates, and that both intragenic and intergenic recombination events are evident. We considered the possibility that the recombinants detected in our analysis were the result of laboratory artifacts, as has been previously suggested [32, 51] . Laboratory contamination is of concern because vaccine derived strains contributed the majority of the recombinant regions and these strains might have been present in laboratories sequencing field aPMV-1 isolates. The presence of unique nucleotide substitutions in the recombinant regions compared to the comparable region of the predicted parental genotypes suggests that these regions did not arise due to contamination with vaccine strains deposited in the sequence databases.