Theory on adaptive genetic robustness under elevated mutation rate generally assumes that phenotype expression results solely from the underlying genotype. However, viruses can employ complementation, a mechanism whereby low-fitness genotypes can use, to their advantage, intracellular proteins made by coinfecting strains of high fitness. [19] [20] [21] Coinfection combined with complementation can therefore provide phenotypic buffering in the event of genomic mutations, similar to other buffering mechanisms such as gene duplication and diploidy that might be positively selected because they facilitate canalization in higher organisms. 22, 23 Complementation can buffer against negative fitness effects of deleterious alleles in coinfecting populations of viruses. 20 This buffering effect introduces an ecologically determined community-level robustness which renders their individuallevel robustness less necessary. This logic infers that the degree of coinfection-high multiplicity of infection ͑MOI; ratio of viruses to cells͒ versus low MOI-should influence evolution of robustness in virus populations. 14 We note that many other phenomena consequential for virus evolution can occur as a result of coinfection, especially genetic exchange ͑recombination͒ between viruses and selection for virus "cheaters" such as defective-interfering particles. 24 For brevity we limit our discussion to complementation that occurs during coinfection and its potential role in the evolution of virus robustness.