Analysis of nuclear and organellar genomes of Plasmodium knowlesi in humans reveals ancient population structure and recent recombination among host-specific subpopulations.
Analysis of nuclear and organellar genomes of Plasmodium knowlesi in humans reveals ancient population structure and recent recombination among host-specific subpopulations.
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DOI：
10.1371/journal.pgen.1007008
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发表时间：
2017-09
期刊：
影响因子：
4.5
通讯作者：
Clark TG
中科院分区：
文献类型：
--
作者：
Diez Benavente E;Florez de Sessions P;Moon RW;Holder AA;Blackman MJ;Roper C;Drakeley CJ;Pain A;Sutherland CJ;Hibberd ML;Campino S;Clark TG
在马来西亚，猕猴寄生虫诺氏疟原虫是一个令人严重担忧的问题，那里的人类感染病例正在增加。感染人类的寄生虫起源于与长尾猕猴(Macaca Fascularis(Mf))或猪尾猕猴(Macaca nomestrina(Mn))相关的不同遗传亚群。我们使用一个新的高质量参考基因组来重新评估先前描述的来自马来西亚婆罗洲和马来西亚半岛的人和猕猴分离株的亚群。正如预期的那样，核基因组是二型性的，但发现了亚群之间染色体片段交换的新证据。在8号染色体上发现了一大段来自MN亚群的片段，该片段包含编码蚊媒寄生虫期表达的蛋白的基因，在Mf基因型中被发现。相比之下，未重组的细胞器基因组分为3个深度分枝的谱系，与核基因组二型性无关。与世隔绝的亚种群重新联系在一起，可能是由于森林砍伐和野生猕猴栖息地的破坏。由此产生的基因组嵌合体揭示了在生态转变的背景下，宿主-病媒-寄生虫相互作用所选择的特征。诺氏疟原虫是一种常见的长尾和猪尾猕猴疟疾寄生虫，现在被认为是人类疟疾的重要原因，在包括马来西亚婆罗洲在内的东南亚某些地区，诺氏疟原虫占疟疾病例的70%。人口的快速增长、森林砍伐和对野生猕猴栖息地的侵占可能会增加与人类的接触，并推高人类诺氏疟原虫感染的流行率。需要适当的分子工具和采样来协助疟疾控制规划的监测，并了解诺氏疟原虫传播和宿主从猕猴向人类转移的遗传学基础。我们报告了来自马来西亚的最大的一组诺氏疟原虫基因组序列的综合分析。它揭示了最近在长尾猕猴和猪尾猕猴之间交换的基因区域，这些区域包含的基因带有指示当代生态快速变化的信号，包括砍伐森林。额外的分析将婆罗洲的诺氏疟原虫感染划分为三个古老的深分支谱系，这发现了与长尾猕猴和猪尾猕猴有关的两个不同种群和第三个高度多样化的种群，位于半岛大陆。总体而言，观察到的复杂的疟原虫进化和进一步宿主转移的可能性是马来西亚疟疾控制的潜在挑战。
The macaque parasite Plasmodium knowlesi is a significant concern in Malaysia where cases of human infection are increasing. Parasites infecting humans originate from genetically distinct subpopulations associated with the long-tailed (Macaca fascicularis (Mf)) or pig-tailed macaques (Macaca nemestrina (Mn)). We used a new high-quality reference genome to re-evaluate previously described subpopulations among human and macaque isolates from Malaysian-Borneo and Peninsular-Malaysia. Nuclear genomes were dimorphic, as expected, but new evidence of chromosomal-segment exchanges between subpopulations was found. A large segment on chromosome 8 originating from the Mn subpopulation and containing genes encoding proteins expressed in mosquito-borne parasite stages, was found in Mf genotypes. By contrast, non-recombining organelle genomes partitioned into 3 deeply branched lineages, unlinked with nuclear genomic dimorphism. Subpopulations which diverged in isolation have re-connected, possibly due to deforestation and disruption of wild macaque habitats. The resulting genomic mosaics reveal traits selected by host-vector-parasite interactions in a setting of ecological transition. Plasmodium knowlesi, a common malaria parasite of long-tailed and pig-tailed macaques, is now recognized as a significant cause of human malaria, accounting for up to 70% of malaria cases in certain areas in Southeast Asia including Malaysian Borneo. Rapid human population growth, deforestation and encroachment on wild macaque habitats potentially increase contact with humans and drive up the prevalence of human Plasmodium knowlesi infections. Appropriate molecular tools and sampling are needed to assist surveillance by malaria control programmes, and to understand the genetics underpinning Plasmodium knowlesi transmission and switching of hosts from macaques to humans. We report a comprehensive analysis of the largest assembled set of Plasmodium knowlesi genome sequences from Malaysia. It reveals genetic regions that have been recently exchanged between long-tailed and pig-tailed macaques, which contain genes with signals indicative of rapid contemporary ecological change, including deforestation. Additional analyses partition Plasmodium knowlesi infections in Borneo into 3 deeply branched lineages of ancient origin, which founded the two divergent populations associated with long-tailed and pig-tailed macaques and a third, highly diverse population, on the Peninsular mainland. Overall, the complex Plasmodium parasite evolution observed and likelihood of further host transitions are potential challenges to malaria control in Malaysia.
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影响因子：
2.7
作者：
Messenger LA;Miles MA
通讯作者：
Miles MA
影响因子：
3.8
作者：
Messenger LA;Llewellyn MS;Bhattacharyya T;Franzén O;Lewis MD;Ramírez JD;Carrasco HJ;Andersson B;Miles MA
通讯作者：
Miles MA
影响因子：
3.7
作者：
Diez Benavente E;Ward Z;Chan W;Mohareb FR;Sutherland CJ;Roper C;Campino S;Clark TG
通讯作者：
Clark TG
DOI：
10.1073/pnas.1522469113
发表时间：
2016-06-28
影响因子：
11.1
作者：
Moon, Robert W.;Sharaf, Hazem;Holder, Anthony A.
通讯作者：
Holder, Anthony A.
影响因子：
3
作者：
Campino, Susana;Benavente, Ernest Diez;Clark, Taane G.
通讯作者：
Clark, Taane G.