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在一个机会主义的人类肺病原体中,De novo突变调解了表型转换

Alexandra J Poret^1,2,3, Matthew Schaefers^4,5, Christina Merakou^4,5

¹Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology.

bioRxiv : the preprint server for biology

|February 19, 2024

概括

囊性纤维化病原体Burkholderia dolosa通过交替O-抗原表达来适应. 损失有助于免疫细胞在感染早期的入侵,而恢复则在慢性阶段受到青,展示了进化灵活性.

科学领域:

微生物学微生物学
进化生物学进化生物学
基因组学就是基因组学.

背景情况:

人类宿主中的细菌面临选择性的权衡,其中的突变可以根据上下文有益或有害.
囊性纤维化相关的病原体Burkholderia dolosa为研究人类感染中的细菌适应提供了一个模型.

研究的目的:

通过连续的点突变,研究Burkholderia dolosa如何通过连续的点突变在人类感染期间克服选择性权衡.
了解O-抗原表达的动态变化及其对不同感染阶段细菌健康的影响.

主要方法:

来自两个最近感染的患者和一个慢性感染的患者的931个呼吸道分离物的全基因组测序.
使用来自同一爆发菌株的112个历史基因组进行比较基因组学.
对O-抗原损失和恢复表型的实验性表征.

主要成果:

在新感染的患者中迅速出现了破坏O抗原表达的多种并行突变,在3年内占据了B. dolosa社区的很大一部分.
发现O-抗原的损失会增加免疫细胞的细菌吸收,但会降低小鼠肺部的竞争力.
这与之前在长期慢性感染期间O抗原恢复突变的研究结果形成鲜明对比.

结论:

Burkholderia dolosa采用突变驱动的表型交替,特别是O-抗原表达,以在人类感染期间导航选择性压力.
O-抗原表达的优势取决于上下文,受组织局部化和感染持续时间的影响.
突变驱动的交替可能是常见但被低估的持续性感染的进化策略,强调需要密集的时间采样.

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