Biology Department, Emory University, Atlanta, GA 30322, USA.
J Evol Biol. 2011 Apr;24(4):712-22. doi: 10.1111/j.1420-9101.2010.02213.x. Epub 2011 Jan 24.
Host resistance to parasites can come in two main forms: hosts may either reduce the probability of parasite infection (anti-infection resistance) or reduce parasite growth after infection has occurred (anti-growth resistance). Both resistance mechanisms are often imperfect, meaning that they do not fully prevent or clear infections. Theoretical work has suggested that imperfect anti-growth resistance can select for higher parasite virulence by favouring faster-growing and more virulent parasites that overcome this resistance. In contrast, imperfect anti-infection resistance is thought not to select for increased parasite virulence, because it is assumed that it reduces the number of hosts that become infected, but not the fitness of parasites in successfully infected hosts. Here, we develop a theoretical model to show that anti-infection resistance can in fact select for higher virulence when such resistance reduces the effective parasite dose that enters a host. Our model is based on a monarch butterfly-parasite system in which larval food plants confer resistance to the monarch host. We carried out an experiment and showed that this environmental resistance is most likely a form of anti-infection resistance, through which toxic food plants reduce the effective dose of parasites that initiates an infection. We used these results to build a mathematical model to investigate the evolutionary consequences of food plant-induced resistance. Our model shows that when the effective infectious dose is reduced, parasites can compensate by evolving a higher per-parasite growth rate, and consequently a higher intrinsic virulence. Our results are relevant to many insect host-parasite systems, in which larval food plants often confer imperfect anti-infection resistance. Our results also suggest that - for parasites where the infectious dose affects the within-host dynamics - vaccines that reduce the effective infectious dose can select for increased parasite virulence.
宿主可以降低寄生虫感染的概率（抗感染抵抗力），或者在感染发生后降低寄生虫的生长速度（抗生长抵抗力）。这两种抵抗机制通常都不完美，这意味着它们不能完全阻止或清除感染。理论工作表明，不完善的抗生长抵抗力可以通过有利于克服这种抵抗力的生长更快、毒性更强的寄生虫来选择更高的寄生虫毒力。相比之下，不完善的抗感染抵抗力被认为不会选择增加寄生虫毒力，因为它假设它减少了感染的宿主数量，但不会影响成功感染的宿主中寄生虫的适应性。在这里，我们开发了一个理论模型，表明当抗感染抵抗力降低进入宿主的有效寄生虫剂量时，它实际上可以选择更高的毒力。我们的模型基于一个帝王蝶-寄生虫系统，其中幼虫的食物植物赋予帝王蝶宿主抗性。我们进行了一项实验，表明这种环境抗性很可能是一种抗感染抵抗力，有毒的食物植物通过这种抵抗力降低了引发感染的寄生虫的有效剂量。我们利用这些结果构建了一个数学模型来研究食物植物诱导的抗性的进化后果。我们的模型表明，当有效感染剂量降低时，寄生虫可以通过进化出更高的每个寄生虫生长速度来补偿，从而产生更高的内在毒力。我们的结果与许多昆虫宿主-寄生虫系统有关，在这些系统中，幼虫的食物植物通常赋予宿主不完善的抗感染抵抗力。我们的结果还表明，对于那些感染剂量影响体内动态的寄生虫来说，减少有效感染剂量的疫苗可能会选择增加寄生虫毒力。
