Department of Population Health and Disease Prevention, University of California, Irvine, CA, 92697, US.
Department of Mathematics, University of California, Irvine, CA, 92697, US.
Nat Commun. 2023 Oct 20;14(1):6642. doi: 10.1038/s41467-023-41787-5.
The literature about mutant invasion and fixation typically assumes populations to exist in isolation from their ecosystem. Yet, populations are part of ecological communities, and enemy-victim (e.g. predator-prey or pathogen-host) interactions are particularly common. We use spatially explicit, computational pathogen-host models (with wild-type and mutant hosts) to re-visit the established theory about mutant fixation, where the pathogen equally attacks both wild-type and mutant individuals. Mutant fitness is assumed to be unrelated to infection. We find that pathogen presence substantially weakens selection, increasing the fixation probability of disadvantageous mutants and decreasing it for advantageous mutants. The magnitude of the effect rises with the infection rate. This occurs because infection induces spatial structures, where mutant and wild-type individuals are mostly spatially separated. Thus, instead of mutant and wild-type individuals competing with each other, it is mutant and wild-type "patches" that compete, resulting in smaller fitness differences and weakened selection. This implies that the deleterious mutant burden in natural populations might be higher than expected from traditional theory.
关于突变体入侵和固定的文献通常假设种群与其生态系统是隔离的。然而，种群是生态群落的一部分，而敌害（例如捕食者-猎物或病原体-宿主）相互作用尤为常见。我们使用空间显式、计算病原体-宿主模型（带有野生型和突变体宿主）重新考察关于突变体固定的已有理论，其中病原体平等地攻击野生型和突变型个体。突变体的适应性与感染无关。我们发现病原体的存在大大削弱了选择，增加了不利突变体的固定概率，降低了有利突变体的固定概率。这种效应的幅度随着感染率的增加而增加。这是因为感染诱导了空间结构，其中突变体和野生型个体在空间上大多是分离的。因此，不是突变体和野生型个体相互竞争，而是突变体和野生型“斑块”相互竞争，导致适应性差异更小，选择作用减弱。这意味着自然种群中的有害突变体负担可能高于传统理论所预期的水平。
