The evolutionary conundrum of pathogen mimicry

A wide range of pathogens use the strategy of mimicking host factors to gain selective advantages at host–pathogen interfaces.Pathogen-encoded mimics can arise by horizontal gene transfer and divergence or independently, by convergent evolution. Some mimics mirror host functions (known as perfect mimicry), whereas others perform different functions (known as imperfect mimicry) to subvert host cellular processes.Mimics impinge on key cellular processes, including the cell cycle, apoptosis, cytoskeletal dynamics, membrane traffic and immunity.Mimicry presents a conundrum to host systems, which must discriminate self from mimics, and also to pathogens, which pay a fitness cost to deploy mimics. Similar trade-offs can influence the evolution of mimicry in ecological settings (for example, insect mimics).Hosts can evolve to counteract mimicry in molecular arms races of adaptations. For example, the antiviral protein kinase R, which is the target of virus-encoded substrate mimics, has a highly flexible interaction interface and adapts on multiple surfaces to disfavour mimics.The extent to which highly conserved cellular factors evolve to counteract mimics is an open question. Several routes seem to be available, including gene duplications followed by functional diversification.