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All alleles at each neutral locus were assumed to be equally related to one another (i.e., an infinite alleles model of mutation was assumed).
An HKY substitution model with back mutation was assumed.
If a SHV peptide was shared among profiles in different complexes, then mutation was assumed when the nucleotide substitution patterns at their SHV differed.
Mutation was assumed to occur following either the stepwise or the infinite-allele model (Kimura 1983), and the fitness of a genotype was assumed to be either 1 or 0 depending on the mutation model and the genotype generated (fig. 9).
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For mutator pathways, the mutator mutation is assumed to occur first, based on previous work suggesting that mutator pathways are more efficient if the mutator mutation occurs early [15].
With this design, the mutation is assumed to be autosomal dominant.
As long as mutation is assumed to be isotropic, only the convergence time to equilibrium, and not the equilibrium fitness value, is affected by the distribution of mutational effects (data not shown).
No backward mutation is assumed.
Mutation is assumed to incur a fitness penalty that reduces the virus production rate k.
Nonsense mediated decay from a heterozygous compound truncating mutation is assumed to be a possible pathogenic mechanism in 439.
Briefly, a given type of event, migration or mutation, is assumed to behave as a Poisson process along a branch.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com