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Genetic characterisation of the erythrocyte-binding protein (PkβII) of Plasmodium knowlesi isolates from Malaysia.
Journal of Genetics ( IF 1.5 ) Pub Date : 2019-09-24
Mun Yik Fong 1 , Yee Ling Lau , Jenarun Jelip , Choo Huck Ooi , Fei Wen Cheong
Affiliation  

Plasmodium knowlesi contributes to the majority of human malaria incidences in Malaysia. Its uncontrollable passage among the natural monkey hosts can potentially lead to zoonotic outbreaks. The merozoite of this parasite invades host erythrocytes through interaction between its erythrocyte-binding proteins (EBPs) and their respective receptor on the erythrocytes. The regionII of P. knowlesi EBP, P. knowlesi beta (PkβII) protein is found to be mediating merozoite invasion into monkey erythrocytes by interacting with sialic acid receptors. Hence, the objective of this study was to investigate the genetic diversity, natural selection and haplotype grouping of PkβII of P. knowlesi isolates in Malaysia. Polymerase chain reaction amplifications of PkβII were performed on archived blood samples from Malaysia and 64 PkβII sequences were obtained. Sequence analysis revealed length polymorphism, and its amino acids at critical residues indicate the ability of PkβII to mediate P. knowlesi invasion into monkey erythrocytes. Low genetic diversity (π = 0.007) was observed in the PkβII of Malaysia Borneo compared to Peninsular Malaysia (π = 0.015). The PkβII was found to be under strong purifying selection to retain infectivity in monkeys and it plays a limited role in the zoonotic potential of P. knowlesi. Its haplotypes could be clustered into Peninsular Malaysia and Malaysia Borneo groups, indicating the existence of two distinct P. knowlesi parasites in Malaysia as reported in an earlier study.

中文翻译:

马来西亚疟原虫分离株的红细胞结合蛋白(PkβII)的遗传表征。

在马来西亚,诺氏疟原虫是导致人类大多数疟疾发病率的原因。它在天然猴子宿主之间的失控传播可能导致人畜共患病暴发。该寄生虫的裂殖子通过其红细胞结合蛋白(EBP)与其在红细胞上的各自受体之间的相互作用侵入宿主红细胞。发现诺氏疟原虫EBP,诺氏疟原虫β(PkβII)蛋白的区域II通过与唾液酸受体相互作用介导裂殖子侵入猴红细胞。因此,本研究的目的是研究马来西亚诺氏疟原虫分离株PkβⅡ的遗传多样性,自然选择和单倍型分组。对来自马来西亚的已归档血液样本进行了PkβII的聚合酶链反应扩增,并获得了64个PkβII序列。序列分析揭示了长度多态性,其关键残基处的氨基酸表明PkβII介导诺氏疟原虫入侵猴子红细胞​​的能力。与马来西亚半岛(π= 0.015)相比,马来西亚婆罗洲的PkβII遗传多样性低(π= 0.007)。已发现PkβII在强纯化作用下可以保留猴子的感染力,并且在诺氏疟原虫的人畜共患病潜力中发挥有限的作用。它的单倍型可以聚类为马来西亚半岛和马来西亚婆罗洲群,这表明马来西亚有两种截然不同的诺氏疟原虫。与马来西亚半岛(π= 0.015)相比,在马来西亚婆罗洲的PkβII中观察到007)。已发现PkβII处于强纯化作用下,可以保留猴子的感染力,并且在诺氏疟原虫的人畜共患病潜力中发挥有限的作用。它的单倍型可以聚类为马来西亚半岛和马来西亚婆罗洲群,这表明马来西亚有两种截然不同的诺氏疟原虫。与马来西亚半岛(π= 0.015)相比,在马来西亚婆罗洲的PkβII中观察到007)。已发现PkβII处于强纯化作用下,可以保留猴子的感染力,并且在诺氏疟原虫的人畜共患病潜力中发挥有限的作用。它的单倍型可以聚类为马来西亚半岛和马来西亚婆罗洲群,这表明马来西亚有两种截然不同的诺氏疟原虫。
更新日期:2019-11-01
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