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Invasion Pathways and Malaria Severity in Kenyan Plasmodium falciparum Clinical Isolates

机译：肯尼亚恶性疟原虫临床分离株的入侵途径和疟疾严重程度

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摘要

The invasion of erythrocytes by Plasmodium falciparum occurs through multiple pathways that can be studied in vitro by examining the invasion of erythrocytes treated with enzymes such as neuraminidase, trypsin, and chymotrypsin. We have studied the invasion pathways used by 31 Kenyan P. falciparum isolates from children with uncomplicated or severe malaria. Six distinct invasion profiles were detected, out of eight possible profiles. The majority of isolates (23 of 31) showed neuraminidase-resistant, trypsin-sensitive invasion, characteristic of the pathway mediated by an unknown parasite ligand and erythrocyte receptor “X.” The neuraminidase-sensitive, trypsin-sensitive phenotype consistent with invasion mediated by the binding of parasite ligand erythrocyte binding antigen 175 to glycophorin A, the most common invasion profile in a previous study of Gambian field isolates, was seen in only 3 of 31 Kenyan isolates. No particular invasion profile was associated with severe P. falciparum malaria, and there was no significant difference in the levels of inhibition by the various enzyme treatments between isolates from children with severe malaria and those from children with uncomplicated malaria (P, >0.1 for all enzymes; Mann-Whitney U test). These results do not support the hypothesis that differences in invasion phenotypes play an important role in malaria virulence and indicate that considerable gaps remain in our knowledge of the molecular basis of invasion pathways in natural P. falciparum infections.
机译：恶性疟原虫对红细胞的侵袭是通过多种途径发生的，可以通过检查神经氨酸酶，胰蛋白酶和胰凝乳蛋白酶等酶对红细胞的侵袭来进行体外研究。我们研究了31个肯尼亚 P所使用的入侵途径。恶性疟原虫从患有简单或严重疟疾的儿童中分离出来。在八个可能的配置文件中检测到六个不同的入侵配置文件。大多数分离株（31个中的23个）显示出对神经氨酸酶抵抗，对胰蛋白酶敏感的侵袭，其特征是由未知的寄生虫配体和红细胞受体“ X”介导。对神经氨酸酶敏感，对胰蛋白酶敏感的表型与由寄生虫配体红细胞结合抗原175与糖蛋白A的结合介导的侵袭一致，这是冈比亚田间分离株先前研究中最常见的侵袭特征，仅在31个肯尼亚分离株中发现了。严重的 P没有特殊的侵袭特征。恶性疟原虫，各种酶处理对重症疟疾患儿和非单纯性疟疾患儿的分离株（ P ，> 0.1所有酶; Mann-Whitney U检验）。这些结果不支持以下假设，即入侵表型的差异在疟疾毒力中起重要作用，并且表明我们对天然P P的入侵途径的分子基础的认识仍存在很大差距。恶性疟原虫感染。

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