非洲锥虫病的发病机制。

Etienne Pays, Magdalena Radwanska, Stefan Magez
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引用次数: 9

摘要

非洲锥虫是一种血液原生动物寄生虫,可感染包括人类在内的哺乳动物,引起昏睡病。寄生虫需要长期感染才能在宿主之间传播。因此,锥虫已经发展出了不断逃避免疫系统先天和适应性反应的策略,同时也防止了宿主的过早死亡。与感染相关的病理主要由炎症引起,除了特异性和抗体反应记忆的丧失外,还包括贫血和脑功能障碍。人类血清中含有一种有效的锥虫分解因子,即膜孔形成蛋白载脂蛋白L1 (APOL1)。在两种人感染性锥虫中,特异性寄生虫耐药因子抑制APOL1活性。反过来,许多非洲人表达APOL1变体,抵消这些抵抗因素,使他们能够避免昏睡病。然而,这些变异与慢性肾脏疾病有关,特别是在2019年冠状病毒病等病毒引起的炎症的情况下。讨论了疫苗接种的观点。
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The Pathogenesis of African Trypanosomiasis.

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.

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来源期刊
CiteScore
62.60
自引率
0.00%
发文量
40
期刊介绍: The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings. In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.
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