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表型变化:生理学在解释噬菌体攻击下细菌持续存在之谜中的作用。

Phenotypic flux: The role of physiology in explaining the conundrum of bacterial persistence amid phage attack.

作者信息

Igler Claudia

机构信息

Department of Environmental Systems Science, ETH Zürich, Institute of Integrative Biology, Universitätstrasse 16, Zurich 8092, Switzerland.

出版信息

Virus Evol. 2022 Sep 15;8(2):veac086. doi: 10.1093/ve/veac086. eCollection 2022.

DOI:10.1093/ve/veac086
PMID:36225237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9547521/
Abstract

Bacteriophages, the viruses of bacteria, have been studied for over a century. They were not only instrumental in laying the foundations of molecular biology, but they are also likely to play crucial roles in shaping our biosphere and may offer a solution to the control of drug-resistant bacterial infections. However, it remains challenging to predict the conditions for bacterial eradication by phage predation, sometimes even under well-defined laboratory conditions, and, most curiously, if the majority of surviving cells are genetically phage-susceptible. Here, I propose that even clonal phage and bacterial populations are generally in a state of continuous 'phenotypic flux', which is caused by transient and nongenetic variation in phage and bacterial physiology. Phenotypic flux can shape phage infection dynamics by reducing the force of infection to an extent that allows for coexistence between phages and susceptible bacteria. Understanding the mechanisms and impact of phenotypic flux may be key to providing a complete picture of phage-bacteria coexistence. I review the empirical evidence for phenotypic variation in phage and bacterial physiology together with the ways they have been modeled and discuss the potential implications of phenotypic flux for ecological and evolutionary dynamics between phages and bacteria, as well as for phage therapy.

摘要

噬菌体,即细菌的病毒,已经被研究了一个多世纪。它们不仅在奠定分子生物学基础方面发挥了重要作用,而且还可能在塑造我们的生物圈中发挥关键作用,并可能为控制耐药细菌感染提供解决方案。然而,预测噬菌体捕食导致细菌根除的条件仍然具有挑战性,有时即使在定义明确的实验室条件下也是如此,而且,最奇怪的是,大多数存活细胞在基因上是否对噬菌体敏感。在这里,我提出即使是克隆的噬菌体和细菌群体通常也处于持续的“表型通量”状态,这是由噬菌体和细菌生理学中的瞬时和非遗传变异引起的。表型通量可以通过将感染力降低到允许噬菌体和易感细菌共存的程度来塑造噬菌体感染动态。理解表型通量的机制和影响可能是全面了解噬菌体与细菌共存的关键。我回顾了噬菌体和细菌生理学中表型变异的经验证据,以及它们被建模的方式,并讨论了表型通量对噬菌体与细菌之间生态和进化动态以及噬菌体治疗的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/b00a7a8a4470/veac086f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/ed7d75a09edb/veac086f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/9051700fe255/veac086f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/b00a7a8a4470/veac086f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/ed7d75a09edb/veac086f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/9051700fe255/veac086f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e88/9547521/b00a7a8a4470/veac086f3.jpg

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