Genetic relationships between parasite virulence and transmission in the rodent malaria Plasmodium chabaudi
Genetic relationships between parasite virulence and transmission in the rodent malaria Plasmodium chabaudi
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DOI：
10.1111/j.1558-5646.1999.tb05364.x
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发表时间：
1999-06-01
期刊：
影响因子：
3.3
通讯作者：
Read, AF
中科院分区：
文献类型：
--
作者：
Mackinnon, MJ;Read, AF
许多寄生虫进化成恶性而不是良性的互利共生者。寄生虫毒力的主要理论模型之一假设，这是因为宿主内的快速复制速率是成功传播（寄生虫适应性）所必需的，并且毒力（对宿主的损害）是这种快速复制的不可避免的后果。这种所谓的进化权衡模型的两个基本假设很少得到经验检验：（1）较高的复制率导致较高的毒力水平;（2）较高的复制率导致较高的传播。这两种关系都必须有一个遗传基础，才能使这种进化假说相关。这些假设进行了测试，在啮齿动物疟疾寄生虫，疟原虫夏氏疟原虫，通过检查从野外分离的8个寄生虫克隆的人口的毒力和传播性状之间的遗传关系。在受控的实验室环境中，将每个克隆注射到近交系小鼠组中，并评估复制率（通过最大无性寄生虫血症测量）、毒力（通过小鼠的活体重损失和贫血程度测量）和传播（通过血液中的性形式、配子体的密度和从小鼠吸血后感染的蚊子的比例测量）。结果发现，克隆在这些性状上差异很大，这些克隆差异在连续的血液传代中是可重复的。毒力性状在表型和遗传上都很强（即，跨克隆）与最大寄生虫血症相关，从而支持快速复制导致更高毒力的第一个假设。传播性状也正表型和遗传相关的寄生虫血症，这支持了第二个假设，即快速复制导致更高的传输。因此，两个假设的寄生虫为中心的权衡模型的毒力的演变被证明是合理的疟疾寄生虫。
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.