Reproductive clonality of pathogens: a perspective on pathogenic viruses, bacteria, fungi, and parasitic protozoa.

We propose that clonal evolution in micropathogens be defined as restrained recombination on an evolutionary scale, with genetic exchange scarce enough to not break the prevalent pattern of clonal population structure, a definition already widely used for all kinds of pathogens, although not clearly formulated by many scientists and rejected by others. The two main manifestations of clonal evolution are strong linkage disequilibrium (LD) and widespread genetic clustering ("near-clading"). We hypothesize that this pattern is not mainly due to natural selection, but originates chiefly from in-built genetic properties of pathogens, which could be ancestral and could function as alternative allelic systems to recombination genes ("clonality/sexuality machinery") to escape recombinational load. The clonal framework of species of pathogens should be ascertained before any analysis of biomedical phenotypes (phylogenetic character mapping). In our opinion, this model provides a conceptual framework for the population genetics of any micropathogen.