...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of the Royal Society Interface >Maintenance of phenotypic diversity within a set of virulence encoding genes of the malaria parasite Plasmodium falciparum
【24h】

Maintenance of phenotypic diversity within a set of virulence encoding genes of the malaria parasite Plasmodium falciparum

机译：在一组疟原虫恶性疟原虫的毒力编码基因中维持表型多样性

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Infection by the human malaria parasite Plasmodium falciparum results in a broad spectrum of clinical outcomes, ranging from severe and potentially life-threatening malaria to asymptomatic carriage. In a process of naturally acquired immunity, individuals living in malaria-endemic regions build up a level of clinical protection, which attenuates infection severity in an exposure-dependent manner. Underlying this shift in the immunoepidemiology as well as the observed range in malaria pathogenesis is the var multigene family and the phenotypic diversity embedded within. The var gene-encoded surface proteins Plasmodium falciparum erythrocyte membrane protein 1 mediate variant-specific binding of infected red blood cells to a diverse set of host receptors that has been linked to specific disease manifestations, including cerebral and pregnancy-associated malaria. Here, we show that cross-reactive immune responses, which minimize the within-host benefit of each additionally expressed gene during infection, can cause selection for maximum phenotypic diversity at the genome level. We further show that differential functional constraints on protein diversification stably maintain uneven ratios between phenotypic groups, in line with empirical observation. Our results thus suggest that the maintenance of phenotypic diversity within P. falciparum is driven by an evolutionary trade-off that optimizes between within-host parasite fitness and between-host selection pressure.
机译：人类疟原虫恶性疟原虫的感染导致广泛的临床结果，从严重的和可能威胁生命的疟疾到无症状的携带。在自然获得的免疫过程中，生活在疟疾流行地区的人们建立了一定的临床保护水平，以依赖于暴露的方式减轻了感染的严重程度。免疫流行病学以及疟疾发病机制中观察到的范围内这一变化的基础是var多基因家族及其内嵌的表型多样性。 var基因编码的表面蛋白恶性疟原虫红细胞膜蛋白1介导了感染红细胞与多种宿主受体的变体特异性结合，所述宿主受体已与特定疾病表现相关，包括脑和妊娠相关的疟疾。在这里，我们显示出交叉反应的免疫反应可以最大程度地减少基因组水平的表型多样性，从而使感染期间每个附加表达的基因的宿主内受益最小化。我们进一步表明，根据经验观察，蛋白质多样化的不同功能限制稳定地维持了表型组之间的不平衡比率。因此，我们的结果表明，恶性疟原虫表型多样性的维持是由进化折衷驱动的，该折衷优化了寄主内寄生虫适应性和寄主间选择压力之间的关系。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号