Mackinnon Margaret J, Read Andrew F
Institute of Cell, Animal and Population Biology, University of Edinburgh, King's Buildings, West Mains Road, Edinburgh, EH9 3JT, United Kingdom.
Evolution. 1999 Jun;53(3):689-703. doi: 10.1111/j.1558-5646.1999.tb05364.x.
Many parasites evolve to become virulent rather than benign mutualists. One of the major theoretical models of parasite virulence postulates that this is because rapid within-host replication rates are necessary for successful transmission (parasite fitness) and that virulence (damage to the host) is an unavoidable consequence of this rapid replication. Two fundamental assumptions underlying this so-called evolutionary trade-off model have rarely been tested empirically: (1) that higher replication rates lead to higher levels of virulence; and (2) that higher replication rates lead to higher transmission. Both of these relationships must have a genetic basis for this evolutionary hypothesis to be relevant. These assumptions were tested in the rodent malaria parasite, Plasmodium chabaudi, by examining genetic relationships between virulence and transmission traits across a population of eight parasite clones isolated from the wild. Each clone was injected into groups of inbred mice in a controlled laboratory environment, and replication rate (measured by maximum asexual parasitemia), virulence (measured by live-weight loss and degree of anemia in the mouse), and transmission (measured by density of sexual forms, gametocytes, in the blood and proportion of mosquitoes infected after taking a blood-meal from the mouse) were assessed. It was found that clones differed widely in these traits and these clone differences were repeatable over successive blood passages. Virulence traits were strongly phenotypically and genetically (i.e., across clones) correlated to maximum parasitemia thus supporting the first assumption that rapid replication causes higher virulence. Transmission traits were also positively phenotypically and genetically correlated to parasitemia, which supports the second assumption that rapid replication leads to higher transmission. Thus, two assumptions of the parasite-centered trade-off model of the evolution of virulence were shown to be justified in malaria parasites.
许多寄生虫会进化成具有毒性的病原体，而非良性共生体。寄生虫毒性的一个主要理论模型假定，这是因为宿主体内的快速复制率是成功传播（寄生虫适应性）所必需的，而毒性（对宿主的损害）是这种快速复制不可避免的结果。这个所谓的进化权衡模型所基于的两个基本假设很少经过实证检验：（1）较高的复制率会导致更高水平的毒性；（2）较高的复制率会导致更高的传播率。要使这个进化假说相关，这两种关系都必须有遗传基础。通过研究从野外分离出的八个寄生虫克隆群体中毒性和传播特征之间的遗传关系，对啮齿动物疟原虫——查巴迪疟原虫的这些假设进行了检验。在可控的实验室环境中，将每个克隆注射到近交系小鼠群体中，并评估复制率（通过最大无性疟原虫血症来衡量）、毒性（通过小鼠体重减轻和贫血程度来衡量）以及传播率（通过血液中性形态配子体的密度以及从小鼠取血后感染的蚊子比例来衡量）。研究发现，这些克隆在这些特征上差异很大，并且这些克隆差异在连续的血液传代中是可重复的。毒性特征在表型和遗传上（即跨克隆）与最大疟原虫血症密切相关，从而支持了第一个假设，即快速复制会导致更高的毒性。传播特征在表型和遗传上也与疟原虫血症呈正相关，这支持了第二个假设，即快速复制会导致更高的传播率。因此，以寄生虫为中心的毒性进化权衡模型的两个假设在疟原虫中被证明是合理的。
