病毒性基因的转录可塑性为疟疾寄生虫提供了更大的适应能力,以避免宿主免疫力
Francesca Florini1, Joseph E Visone1, Evi Hadjimichael1
1Department of Microbiology and Immunology, Weill Cornell Medical College, New York, New York, USA.
bioRxiv : the preprint server for biology
|March 18, 2024
概括
慢性疟疾感染通过改变Plasmodium falciparum var基因表达而持续存在. 寄生虫可以表达多个var基因或没有任何基因,逃避免疫检测并阻碍疟疾根除工作.
科学领域:
- 疟疾学 疟疾学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 慢性无症状的疟疾感染是消除疟疾的主要障碍.
- 杆菌 (Plasmodium falciparum) 通过切换多种基因表达来逃避免疫检测,在感染的红细胞上编码表面抗原.
- 这种免疫规避可以使感染延长数年,从而为传播创造一个储存库.
研究的目的:
- 在慢性无症状感染期间,研究寄生虫Plasmodium falciparum在免疫学上保持"隐形"的机制.
- 挑战现有的相互排斥的多种基因表达模式.
主要方法:
- 在Plasmodium falciparum中分析各种基因表达模式.
- 研究寄生虫的转录灵活性.
主要成果:
- 寄生虫可以同时表达多个var基因,这与公认的单基因表达模型相反.
- 寄生虫也可以进入极少或完全无法检测到的多种基因表达的状态.
- 这表明,与以前理解的不同基因表达的适应能力和灵活性更大.
结论:
- 这些发现挑战了Plasmodium falciparum中相互排斥的多种基因表达的教条.
- 变异基因表达的不被赞赏的灵活性解释了寄生虫在长期无症状感染期间如何在抗原上保持"隐形".
- 了解这些机制对于制定消除疟疾的战略至关重要.
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