The circular, double-stranded 8-kb DNA genome of papillomaviruses (PVes) consists mainly of 4 large genes, E1, E2, L2, and L1. Approximately 150 papillomavirus genomes have been sequenced to date. We analyzed a representative sample of 53 PVes genomes using maximum likelihood, Bayesian inference, maximum parsimony, and distance-based methods both on nucleotide (nt) and on amino acid (aa) alignments. When the 4 genes were analyzed separately, aa-inferred phylogenies contradicted each other less than nt-inferred trees (judged by partition homogeneity tests). In particular, gene combinations including the L2 gene generated significant incongruence (P < 0.001). Combined analyses of the remaining genes E1-E2-L1 produced a well-supported phylogeny including supertaxon β + γ + π + ξ-PVes (infecting Artiodactyla, Carnivora, Primates, and Rodentia) and supertaxon κ + λ + μ + ν + σ-PVes (infecting Carnivora, Lagomorpha, Primates, and Rodentia). Based on the tree topology, host-linked evolution appears plausible at shallow, rather than deeper, taxonomic levels. Diversification within PVes may also involve adaptive radiation establishing different niches (within a single-host species) and recombination events (within single-host cells). Heterogeneous groups of closely related PVes infecting, for example, humans and domestic animals such as hamster, dog, and cattle suggest multiple infections across species borders. Additional evolutionary phenomena such as strong codon usage preferences, and computational biases including reconstruction artifacts and insufficient taxon sampling, may contribute to the incomplete resolution of deep phylogenetic nodes. The molecular data globally supports a complex evolutionary scenario for PVes, which is driven by multiple mechanisms but not exclusively by coevolution with corresponding hosts. © The Author 2007. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. All rights reserved.
CITATION STYLE
Gottschling, M., Stamatakis, A., Nindl, I., Stockfleth, E., Alonso, Á., & Bravo, I. G. (2007). Multiple evolutionary mechanisms drive papillomavirus diversification. Molecular Biology and Evolution, 24(5), 1242–1258. https://doi.org/10.1093/molbev/msm039
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