Is Predominant Clonal Evolution a Common Evolutionary Adaptation to Parasitism in Pathogenic Parasitic Protozoa, Fungi, Bacteria, and Viruses?
We propose that predominant clonal evolution (PCE) in microbial pathogens be defined as restrained recombination on an evolutionary scale, with genetic exchange scarce enough to not break the prevalent pattern of clonal population structure. The main features of PCE are (1) strong linkage disequilibrium, (2) the widespread occurrence of stable genetic clusters blurred by occasional bouts of genetic exchange ('near-clades'), (3) the existence of a "clonality threshold", beyond which recombination is efficiently countered by PCE, and near-clades irreversibly diverge. We hypothesize that the PCE features are not mainly due to natural selection but also chiefly originate from in-built genetic properties of pathogens. We show that the PCE model obtains even in microbes that have been considered as 'highly recombining', such as Neisseria meningitidis, and that some clonality features are observed even in Plasmodium, which has been long described as panmictic. Lastly, we provide evidence that PCE features are also observed in viruses, taking into account their extremely fast genetic turnover. The PCE model provides a convenient population genetic framework for any kind of micropathogen. It makes it possible to describe convenient units of analysis (clones and near-clades) for all applied studies. Due to PCE features, these units of analysis are stable in space and time, and clearly delimited. The PCE model opens up the possibility of revisiting the problem of species definition in these organisms. We hypothesize that PCE constitutes a major evolutionary strategy for protozoa, fungi, bacteria, and viruses to adapt to parasitism.
Institut de Recherche pour le Développement, Montpellier, France.
M
M
Tibayrenc
University of California at Irvine, United States.
F J
FJ
Ayala
D000222:Adaptation, Physiological; D000818:Animals; D001419:Bacteria / Q000235:genetics* / Q000528:radiation effects; D005075:Biological Evolution; D060965:Clonal Evolution; D005658:Fungi / Q000235:genetics* / Q000502:physiology; D006801:Humans; D015810:Linkage Disequilibrium; D010271:Parasites / Q000235:genetics* / Q000502:physiology; D014780:Viruses / Q000235:genetics*
Aneuploidy; Clonality; Clone; Cryptococcus; HIV; Leishmania; Linkage disequilibrium; Molecular epidemiology; Near-clade; Neisseria; Plasmodium; Restrained recombination; Toxoplasma; Trypanosoma