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The Pathogenesis of African Trypanosomiasis
Annual Review of Pathology: Mechanisms of Disease ( IF 28.4 ) Pub Date : 2022-09-03 , DOI: 10.1146/annurev-pathmechdis-031621-025153
Etienne Pays 1 , Magdalena Radwanska 2, 3 , Stefan Magez 2, 4, 5
Affiliation  

African trypanosomes are bloodstream protozoan parasites that infect mammals including humans, where they cause sleeping sickness. Long-lasting infection is required to favor parasite transmission between hosts. Therefore, trypanosomes have developed strategies to continuously escape innate and adaptive responses of the immune system, while also preventing premature death of the host. The pathology linked to infection mainly results from inflammation and includes anemia and brain dysfunction in addition to loss of specificity and memory of the antibody response. The serum of humans contains an efficient trypanolytic factor, the membrane pore-forming protein apolipoprotein L1 (APOL1). In the two human-infective trypanosomes, specific parasite resistance factors inhibit APOL1 activity. In turn, many African individuals express APOL1 variants that counteract these resistance factors, enabling them to avoid sleeping sickness. However, these variants are associated with chronic kidney disease, particularly in the context of virus-induced inflammation such as coronavirus disease 2019. Vaccination perspectives are discussed.

中文翻译:


非洲锥虫病的发病机制



非洲锥虫是血液原生动物寄生虫,可感染包括人类在内的哺乳动物,并引起昏睡病。需要持久的感染才能促进寄生虫在宿主之间的传播。因此,锥虫已经开发出不断逃避免疫系统的先天性和适应性反应的策略,同时还可以防止宿主过早死亡。与感染相关的病理主要由炎症引起,除了抗体反应的特异性和记忆丧失外,还包括贫血和脑功能障碍。人类血清含有一种有效的锥虫溶解因子,即膜成孔蛋白载脂蛋白 L1 (APOL1)。在两种人类感染性锥虫中,特异性寄生虫抗性因子抑制 APOL1 活性。反过来,许多非洲个体表达抵消这些抵抗因子的 APOL1 变体,使他们能够避免昏睡病。然而,这些变异与慢性肾病有关,尤其是在病毒诱导的炎症(如 2019 冠状病毒病)的情况下。讨论了疫苗接种的观点。
更新日期:2022-09-03
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