Abstract
Resistance spreads rapidly in pathogen or pest populations exposed to biocides, such as fungicides and antibiotics, and in many cases new biocides are in short supply. How can resistance be reversed in order to prolong the effectiveness of available treatments? Some key parameters affecting reversion of resistance are well known, such as the fitness cost of resistance. However, the population biological processes that actually cause resistance to persist or decline remain poorly characterized, and consequently our ability to manage reversion of resistance is limited. Where do susceptible genotypes that replace resistant lineages come from? What is the epidemiological scale of reversion? What information do we need to predict the mechanisms or likelihood of reversion? Here, we define some of the population biological processes that can drive reversion, using examples from a wide range of taxa and biocides. These processes differ primarily in the origin of revertant genotypes, but also in their sensitivity to factors such as coselection and compensatory evolution that can alter the rate of reversion, and the likelihood that resistance will re-emerge upon re-exposure to biocides. We therefore argue that discriminating among different types of reversion allows for better prediction of where resistance is most likely to persist.
Highlights
Resistance to a given biocide, such as an antibiotic or fungicide, can decline in frequency in populations no longer exposed to it (e.g. [1,2,3,4]), but often does not (e.g. [5,6,7,8])
The plant pathologists working on C. beticola generate resistance maps annually to identify geographical hotspots of resistance to particular fungicides, and sugar beet growers in these hotspots are encouraged to use fungicides with a different mode of action in the following year to enable a reversion of resistance
The reversibility of resistance in HIV-1 appears to vary among resistance alleles and may be explained by multiple factors, including high mutation rate [40], fitness costs associated with resistance [41], and that resistance can be encoded by a single amino acid change, meaning that a single mutation can restore the wild-type allele [42]
Summary
Resistance to a given biocide, such as an antibiotic or fungicide, can decline in frequency in populations no longer exposed to it (e.g. [1,2,3,4]), but often does not (e.g. [5,6,7,8]). Some evolutionary processes and genetic factors that alter the likelihood of reversion have been identified (e.g. coselection, costs of resistance, compensatory adaptation) and studied for specific resistance mechanisms in controlled experiments. [9]), in real-world pathogens and pests Across systems it is unclear why reversion is more likely for some resistance mechanisms and ecological scenarios than others. We aim to alert researchers studying resistance in individual species or scenarios to mechanisms of reversion that may be important but so far only observed elsewhere. Lineage that decrease resistance without restoring the ancestral genotype, (iii) replacement of resistant genotypes by less resistant genotypes of the same species or strain that are not derived from the ancestral population We refer to these processes as isogenetic, paragenetic, and allogenetic reversion, respectively (figure 1), reflecting the different types of genetic variation involved. The population biological processes by which costs of resistance translate to a net reduction in average resistance have received much less attention, and that is our focus here
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