人类伊氏锥虫感染与载脂蛋白L-I缺乏有关。
Human Trypanosoma evansi infection linked to a lack of apolipoprotein L-I.
作者信息
Vanhollebeke Benoit, Truc Philippe, Poelvoorde Philippe, Pays Annette, Joshi Prashant P, Katti Ravindra, Jannin Jean G, Pays Etienne
机构信息
Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires, Université Libre de Bruxelles, Gosselies, Belgium.
出版信息
N Engl J Med. 2006 Dec 28;355(26):2752-6. doi: 10.1056/NEJMoa063265.
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.
人类对布氏布氏锥虫具有先天性免疫，已知该免疫涉及载脂蛋白L-I（APOL1）。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途径是否与这一事件有关。发现感染患者的血清没有溶锥虫活性，这一发现与APOL1的缺乏有关，而APOL1的缺乏是由于两个APOL1等位基因发生了移码突变。通过添加重组APOL1恢复了溶锥虫活性。APOL1的缺乏解释了该患者感染伊氏锥虫的原因。
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