Genetic diversity and population structure of Plasmodium falciparum in Thailand, a low transmission country.
Genetic diversity and population structure of Plasmodium falciparum in Thailand, a low transmission country.
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DOI：
10.1186/1475-2875-8-155
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发表时间：
2009-07-14
期刊：
影响因子：
3
通讯作者：
Harnyuttanakorn P
中科院分区：
文献类型：
--
作者：
Pumpaibool T;Arnathau C;Durand P;Kanchanakhan N;Siripoon N;Suegorn A;Sitthi-Amorn C;Renaud F;Harnyuttanakorn P
人类疟疾的病原体，包括最严重的恶性疟原虫，其种群结构取决于当地的流行病学和人口学情况，如感染者的发病率、媒介传播强度和居民的迁移(即地点之间的交流)。在大陆等大范围分析恶性疟原虫种群结构，或使用非中性选择的标记，可能会导致对有效传播过程的掩盖和误解。因此，需要了解具有中性遗传标记的特定地区恶性疟原虫种群的遗传结构和组织，以了解哪些流行病学因素应该作为疾病控制的目标。关于泰国恶性疟原虫种群遗传多样性和结构的报告有限，这在泰国-缅甸和泰国-柬埔寨边境特别令人关切，据报道，这些地区对甲氟喹等抗疟疾药物具有很高的耐药性，对其潜在的基因流动几乎不了解。利用分布在14条不同染色体上的8条染色体上的12个明显中性的多态微卫星座位，分析了恶性疟原虫种群的多样性和遗传分化。样本来自泰国西部、东部和南部的七个省。观察到大多数被测群体在核遗传结构上存在很大差异。遗传多样性与恶性疟原虫低传播区的中等水平相当(平均HS=0.65±0.17)，南美洲最低，非洲最高。然而，雅拉省独一无二，在所有样本中只有一个多位基因座基因型，导致在本研究期间与其他泰国人群相比存在强烈的地理差异。泰国恶性疟原虫种群与法属圭亚那、刚果和喀麦隆恶性疟原虫种群的遗传结构比较表明，除这两个非洲国家外，其他三个国家的恶性疟原虫种群间均存在显著的遗传分化，而各国间的恶性疟原虫遗传变异表现为重叠分布。恶性疟原虫显示了泰国当地地区的遗传结构种群。虽然泰国被认为是一个低传播区，但在所研究的五个地区中，发现了相对较高的遗传多样性水平，没有发现连锁不平衡，但雅拉省(泰国南部半岛)和坎察那武里省(泰国西部)除外，那里发现了克隆种群结构。这一发现在疟疾控制方面特别重要，因为它有助于了解不同用药史和不同用药方法地区寄生虫种群的特殊动态。
The population structure of the causative agents of human malaria, Plasmodium sp., including the most serious agent Plasmodium falciparum, depends on the local epidemiological and demographic situations, such as the incidence of infected people, the vector transmission intensity and migration of inhabitants (i.e. exchange between sites). Analysing the structure of P. falciparum populations at a large scale, such as continents, or with markers that are subject to non-neutral selection, can lead to a masking and misunderstanding of the effective process of transmission. Thus, knowledge of the genetic structure and organization of P. falciparum populations in a particular area with neutral genetic markers is needed to understand which epidemiological factors should be targeted for disease control. Limited reports are available on the population genetic diversity and structure of P. falciparum in Thailand, and this is of particular concern at the Thai-Myanmar and Thai-Cambodian borders, where there is a reported high resistance to anti-malarial drugs, for example mefloquine, with little understanding of its potential gene flow. The diversity and genetic differentiation of P. falciparum populations were analysed using 12 polymorphic apparently neutral microsatellite loci distributed on eight of the 14 different chromosomes. Samples were collected from seven provinces in the western, eastern and southern parts of Thailand. A strong difference in the nuclear genetic structure was observed between most of the assayed populations. The genetic diversity was comparable to the intermediate level observed in low P. falciparum transmission areas (average HS = 0.65 ± 0.17), where the lowest is observed in South America and the highest in Africa. However, uniquely the Yala province, had only a single multilocus genotype present in all samples, leading to a strong geographic differentiation when compared to the other Thai populations during this study. Comparison of the genetic structure of P. falciparum populations in Thailand with those in the French Guyana, Congo and Cameroon revealed a significant genetic differentiation between all of them, except the two African countries, whilst the genetic variability of P. falciparum amongst countries showed overlapping distributions. Plasmodium falciparum shows genetically structured populations across local areas of Thailand. Although Thailand is considered to be a low transmission area, a relatively high level of genetic diversity and no linkage disequilibrium was found in five of the studied areas, the exception being the Yala province (Southern peninsular Thailand), where a clonal population structure was revealed and in Kanchanaburi province (Western Thailand). This finding is particularly relevant in the context of malaria control, because it could help in understanding the special dynamics of parasite populations in areas with different histories of, and exposure to, drug regimens.
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影响因子：
3.6
作者：
Healer, J;Murphy, V;Batchelor, A
通讯作者：
Batchelor, A
DOI：
10.1073/pnas.0500078102
发表时间：
2005-05-24
影响因子：
11.1
作者：
de Roode, JC;Pansini, R;Read, AF
通讯作者：
Read, AF
DOI：
10.1073/pnas.0702715104
发表时间：
2007-05-08
影响因子：
11.1
作者：
Annan, Zeinab;Durand, Patrick;Renaud, Francois
通讯作者：
Renaud, Francois
影响因子：
3.2
作者：
Ariey, Frederic;Duchemin, Jean-Bernard;Robert, Vincent
通讯作者：
Robert, Vincent
影响因子：
3.8
作者：
O'Loughlin, S. M.;Somboon, P.;Walton, C.
通讯作者：
Walton, C.