Genetic diversity in twenty variants of the avian polyomavirus

To determine if different pathotypes of the avian polyomavirus (APV) exist and to compare the genomes of APVs originating from different geographic ar eas, dates, and species of birds, the partial sequences of 18 APVs were det ermined. New viral sequences were compared with three published APV sequenc es. Two of the new viruses had identical sequences. Forty point mutations w ere found at 31 loci. A 27-bp deletion was found in the VP2 and VP3 open re ading frames of one virus. A duplication of the putative origin of replicat ion and adjacent enhancer region was previously reported in one APV. Smalle r duplications involving the origin in one APV and a second enhancer region in another were discovered. All duplications were in tissue culture-adapte d viruses, suggesting they occurred during the isolation process. Excluding duplications and the deletion, maximum variation between viruses was small (11 bp). A maximum parsimony tree was constructed that contained three maj or branches. The three earliest isolates were on separate branches. The Eur opean viruses were confined to branch I, but APVs from the United States we re on all three branches. Lovebird, budgerigar, and macaw APVs were also on each of the three branches, suggesting that species-specific pathotypes ha ve not developed. Most nonsynonymous mutations occurred in a small portion of the VP2 and VP3 open reading frames, demonstrating a selection for these mutations. That a glycine at VP2 221 will inhibit virus replication in chi cken embryo fibroblasts (CEFs) has been previously reported. In contrast, s ix of seven of the new APVs isolated in CEFs had a glycine at VP2 221.