Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.

Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.
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DOI:
10.1038/s41579-018-0013-4
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发表时间:
2018-08
期刊:
Nature reviews. Microbiology
影响因子:
--
通讯作者:
Rhee KY
Rhee KY
中科院分区:
其他
文献类型:
--
作者:
Ehrt S;Schnappinger D;Rhee KY

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一旦降级的能量和生物合成前体的供应,它现在已经变得清楚,代谢是几乎所有生理过程的特定介质。在微生物发病机制的背景下,代谢已经扩展到其在细菌复制中的典型作用之外。在人类病原体中,这种扩张可能比结核病的病原体结核分枝杆菌更明显。与大多数病原体不同,M.结核病是在人体内演变而来的,人体既是宿主又是贮存者。这使得无限制的复制和永久的静止同样不相容的生存策略作为一个物种。在这篇综述中,我们总结了最近的工作,说明了代谢功能的多样性,不仅使M。结核病在宿主体内建立和维持慢性感染状态,也有利于在药物压力下生存,并最终完成其生命周期。
Once relegated to the supply of energy and biosynthetic precursors, it has now become clear that metabolism is a specific mediator of nearly all physiologic processes. In the context of microbial pathogenesis, metabolism has expanded outside its canonical role in bacterial replication. Among human pathogens, this expansion has emerged perhaps nowhere more visibly than for Mycobacterium tuberculosis, the causative agent of tuberculosis. Unlike most pathogens, M. tuberculosis has evolved within humans, which are both host and reservoir. This makes unrestrained replication and perpetual quiescence equally incompatible strategies for survival as a species. In this Review, we summarize recent work that illustrates the diversity of metabolic functions that not only enable M. tuberculosis to establish and maintain a state of chronic infection within the host, but also facilitate survival in the face of drug pressure and, ultimately, completion of its life cycle.
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