Brief report:: Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I
Brief report:: Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I
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DOI：
10.1056/nejmoa063265
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发表时间：
2006-12-28
影响因子：
158.5
通讯作者：
Pays, Etienne
中科院分区：
文献类型：
--
作者：
Vanhollebeke, Benoit;Truc, Philippe;Pays, Etienne
人类对布鲁氏锥虫具有天然免疫力，这种免疫力与载脂蛋白L-I(Apo1)有关。最近，在印度发现了一例人类感染伊氏锥虫的病例。我们调查了APOL1通路是否参与了这一事件。感染患者的血清被发现没有胰酶溶解活性，这一发现与缺乏APOL1有关，这是由于两个APOL1等位基因的移码突变所致。加入重组APOL1可恢复胰酶的降解活性。APOL1的缺失解释了患者感染伊氏锥虫的原因。
Humans have innate immunity against Trypanosoma brucei brucei that is known to involve apolipoprotein L-I (APOL1). Recently, a case of T. evansi infection in a human was identified in India. We investigated whether the APOL1 pathway was involved in this occurrence. The serum of the infected patient was found to have no trypanolytic activity, and the finding was linked to the lack of APOL1, which was due to frameshift mutations in both APOL1 alleles. Trypanolytic activity was restored by the addition of recombinant APOL1. The lack of APOL1 explained the patient's infection with T. evansi.