Synonymous nucleotide changes drive papillomavirus evolution

Genetic Drift and <em>Alphapapillomavirus</em> Evolution

“…These results are most consistent with a non-random mutation burden associated with genetic drift [88,89]. Given the rarity of positive Darwinian selection [26] and recombination, new HPV variants emerge containing different combinations of non-coding elements as we describe from our analysis of 13 higher-order nucleotide motifs. Surprisingly, even nucleotide composition alone discriminated closely related types, e.g., alpha-9 types (compare Figure 3A/B and Figure 5).…”

“…Thus, current evidence for selection or its counterpart genetic drift are hampered by few analytical methods. Whole genome analyses of various HPV types do not support the notion that pathogenicity is more strongly connected to nonsynonymous substitutions [26] than perhaps to a lack thereof [27][28][29] or to other kinds of substitution in papillomavirus genomes [29,30]. Indeed, elevated oncogenic risk from large epidemiological studies is also associated with variation in noncoding regions and with silent substitutions that are non-randomly distributed across the ~8000 bp genome [30][31][32][33].…”

Distinguishing Genetic Drift from Selection in Papillomavirus Evolution

“…These results are most consistent with directional mutation pressure and neutral evolution (i.e., genetic drift as described by Sueoka [ 97 , 98 ]). Given the rarity of positive Darwinian selection [ 26 ] and recombination, new HPV variants emerge containing different combinations of non-coding motifs as we describe from our analysis of 13 higher-order nucleotide motifs. Surprisingly, even nucleotide composition alone discriminated closely related types, e.g., alpha-9 types (compare Figure 3 and Figure 5 ).…”

“…Thus, current evidence for selection or its alternative, genetic drift, are hampered by few analytical methods. Whole genome analyses of various HPV types do not support the notion that pathogenicity is more strongly connected to nonsynonymous substitutions [26] than, perhaps, to a lack thereof [27][28][29] or to other kinds of substitution…”

“…Thus, current evidence for selection or its alternative, genetic drift, are hampered by few analytical methods. Whole genome analyses of various HPV types do not support the notion that pathogenicity is more strongly connected to nonsynonymous substitutions [ 26 ] than, perhaps, to a lack thereof [ 27 , 28 , 29 ] or to other kinds of substitution in papillomavirus genomes [ 29 , 30 ]. Indeed, elevated oncogenic risk from large epidemiological studies is also associated with variations in non-coding regions and with silent substitutions that are non-randomly distributed across the ~8000 bp genome [ 30 , 31 , 32 , 33 ].…”