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<p>Host genetic variability strongly shapes virus evolution by defining the selective pressures that drive pathogens to either diversify across resistance alleles or specialize on the most susceptible genotypes. These dynamics can also shift virulence, though the direction of change is not always predictable. Experimental evolution with potyviruses in different <i>Arabidopsis thaliana</i> genotypes offers clear evidence. Across genotypes classified as permissive, wild-type-like, or restrictive, adaptation proceeded faster in restrictive hosts than in permissive ones. Cross-infection assays showed that restrictive genotypes favored generalist viruses able to overcome multiple barriers, whereas permissive genotypes selected specialists optimized for high fitness in a single host. Together, these results highlight how host heterogeneity —whether from natural variation, targeted mutations, or epigenetic regulation— determines the tempo and mode of virus evolution, with implications for predicting pathogen emergence and designing durable resistance strategies.</p>

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From basal defenses to chromatin landscapes: how Arabidopsis genetic diversity modulates potyvirus evolutionary dynamics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月27日

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  • Santiago F. Elena

摘要

Host genetic variability strongly shapes virus evolution by defining the selective pressures that drive pathogens to either diversify across resistance alleles or specialize on the most susceptible genotypes. These dynamics can also shift virulence, though the direction of change is not always predictable. Experimental evolution with potyviruses in different Arabidopsis thaliana genotypes offers clear evidence. Across genotypes classified as permissive, wild-type-like, or restrictive, adaptation proceeded faster in restrictive hosts than in permissive ones. Cross-infection assays showed that restrictive genotypes favored generalist viruses able to overcome multiple barriers, whereas permissive genotypes selected specialists optimized for high fitness in a single host. Together, these results highlight how host heterogeneity —whether from natural variation, targeted mutations, or epigenetic regulation— determines the tempo and mode of virus evolution, with implications for predicting pathogen emergence and designing durable resistance strategies.