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首页> 外文期刊>Parasitology >Searching for virulence factors in the non-pathogenic parasite to humans Leishmania tarentolae.
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Searching for virulence factors in the non-pathogenic parasite to humans Leishmania tarentolae.

机译：在对人类利什曼原虫的非致病性寄生虫中寻找毒力因子。

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Leishmania protozoa are obligate intracellular parasites that reside in the phagolysosome of host macrophages and cause a large spectrum of pathologies to humans known as leishmaniases. The outcome of the disease is highly dependent on the parasite species and on its ascribed virulence factors and the immune status of the host. Characterization of the genome composition of non-pathogenic species could ultimately open new horizons in Leishmania developmental biology and also the disease monitoring. Here, we provide evidence that the lizard non-pathogenic to humans Leishmania tarentolae species expresses an Amastin-like gene, cysteine protease B (CPB), lipophosphoglycan LPG3 and the leishmanolysin GP63, genes well-known for their potential role in the parasite virulence. These genes were expressed at levels comparable to those in L. major and L. infantum both at the level of mRNA and protein. Alignment of the L. tarentolae proteins with their counterparts in the pathogenic species demonstrated that the degree of similarity varied from 59% and 60% for Amastin, 89% for LPG3 and 71% and 68% for CPB, in L. major and L. infantum, respectively. Interestingly, the A2 gene, expressed specifically by the L. donovani complex which promotes visceralization, was absent in L. tarentolae. These findings suggest that the lack of pathogenicity in L. tarentolae is not associated with known virulence genes such as LPG3, CPB, GP63 and Amastin, and that other factors either unique to L. tarentolae or missing from this species may be responsible for the non-pathogenic potential of this lizard parasite.
机译：利什曼原虫是专性的细胞内寄生虫，其位于宿主巨噬细胞的吞噬体中，并引起人类广泛的病理学，称为利什曼原虫病。该疾病的结果高度依赖于寄生虫种类及其归因于其的毒力因子和宿主的免疫状况。非致病性物种的基因组组成的表征最终可以为利什曼原虫发育生物学以及疾病监测开辟新的视野。在这里，我们提供证据表明对人类利什曼原虫的非致病性蜥蜴表达一种Amastin样基因，半胱氨酸蛋白酶B（CPB），脂蛋白聚糖LPG3和Leishmanolysin GP63，这些基因因其在寄生虫毒力中的潜在作用而闻名。这些基因在mRNA和蛋白质水平上的表达水平均与大麦草和婴儿乳杆菌中的水平相当。塔氏乳杆菌蛋白与其致病物种中的对应物的比对表明，在L. major和L.中，相似度的变化程度从阿马斯汀的59％和60％，LPG3的89％和CPB的71％和68％不等。婴儿。有趣的是，在塔伦支乳杆菌中不存在由促进内脏化的杜氏乳杆菌复合体特异性表达的A2基因。这些发现表明，塔伦特氏菌缺乏致病性与已知的毒力基因（例如LPG3，CPB，GP63和Amastin）无关，并且塔伦特氏菌特有的其他因素或该物种缺失的其他因素可能是造成这种疾病的原因。蜥蜴寄生虫的致病潜力。

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