Persistence is a state of bacterial dormancy where cells with low metabolic activity and growth rates are phenotypically tolerant to antibiotics and other cytotoxic substances. Given its obvious advantage to bacteria, several researchers have been looking for the genetic mechanism behind persistence. However, other authors argue that there is no such mechanism and that persistence results from inadvertent cell errors. In this case, the persistent population should decay according to a power-law with a particular exponent of -2. Studying persisters' decay is, therefore, a valuable way to understand persistence. Here we simulated the fate of susceptible cells in laboratory experiments in the context of indirect resistance. Eventually, under indirect resistance, detoxifying drug-resistant cells save the persister cells that leave the dormant state and resume growth. The simulations presented here show that, by assuming a power-law decline, the exponent is close to -2, which is the expected value if persistence results from unintentional errors. Whether persisters are cells in a moribund state or, on the contrary, result from a genetic program, should impact the research of anti-persistent drugs.

中文翻译：

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缓慢死亡的力量-持久性为意外休眠

持久性是细菌休眠的一种状态，其中具有低代谢活性和生长速率的细胞在表型上可以耐受抗生素和其他细胞毒性物质。鉴于其对细菌的明显优势，一些研究人员一直在寻找持久性背后的遗传机制。但是，其他作者则认为没有这种机制，并且持久性是由无意中的单元错误导致的。在这种情况下，持久人口应根据幂指数（具有-2的特定指数）衰减。因此，研究持久性的衰变是了解持久性的一种有价值的方法。在这里，我们在间接抵抗的背景下，在实验室实验中模拟了易感细胞的命运。最终，在间接的抵抗下，排毒的抗药性细胞保存了保持休眠状态的持久性细胞并恢复生长。此处给出的仿真结果表明，假设幂律下降，则指数接近-2，如果持久性是由于意外错误而导致的，则该期望值为-2。持久性细胞是处于垂死状态的细胞，还是相反地是由遗传程序产生的细胞，都将影响抗持久性药物的研究。