可以说,对细菌最大的威胁是噬菌体。通常认为那些逃避噬菌体感染的细菌已经突变或利用了噬菌体防御系统;然而,另一种可能性是,亚群以类似于细菌细胞经历营养的方式形成休眠持久状态,氧化,抗生素压力。支持细胞不发生突变,并通过暂时停止生长而在致死条件下存活。较慢的生长和休眠起着关键的生理作用,因为它们允许宿主噬菌体防御系统有更多的时间来清除噬菌体感染。这里,我们通过从T2,T4和lambda(cI突变体)毒力噬菌体的噬斑中分离存活细胞并对其基因组进行测序,研究了细菌如何在裂解性噬菌体感染中存活.我们发现,噬斑中的细菌可以通过突变(即变得抗性)和没有突变(即变得持久)而逃避噬菌体攻击。具体来说,而敏感性低于100,000倍以上的T4抗性和λ抗性细菌是从具有明显遗传突变(例如引起粘膜样)的斑块中分离出来的,在T2感染后也发现了没有明显突变的细胞,保留野生型噬菌体敏感性,并在致命剂量的抗生素中存活。证实这一点,与指数生长的细胞相比,将T2噬菌体添加到持久细胞中可使存活率提高137,000倍。此外,我们的结果似乎很普遍,因为用肺炎克雷伯菌和铜绿假单胞菌进行噬菌体处理也会产生持久细胞.因此,连同抗性菌株,在噬菌体感染过程中,细菌也会形成持久细胞。
Arguably, the greatest threat to bacteria is phages. It is often assumed that those bacteria that escape phage infection have mutated or utilized phage-defence systems; however, another possibility is that a subpopulation forms the dormant persister state in a manner similar to that demonstrated for bacterial cells undergoing nutritive, oxidative, and antibiotic stress. Persister cells do not undergo mutation and survive lethal conditions by ceasing growth transiently. Slower growth and dormancy play a key physiological role as they allow host phage defence systems more time to clear the phage infection. Here, we investigated how bacteria survive lytic phage infection by isolating surviving cells from the plaques of T2, T4, and lambda (cI mutant) virulent phages and sequencing their genomes. We found that bacteria in plaques can escape phage attack both by mutation (i.e. become resistant) and without mutation (i.e. become persistent). Specifically, whereas T4-resistant and lambda-resistant bacteria with over a 100,000-fold less sensitivity were isolated from plaques with obvious genetic mutations (e.g. causing mucoidy), cells were also found after T2 infection that undergo no significant mutation, retain wild-type phage sensitivity, and survive lethal doses of antibiotics. Corroborating this, adding T2 phage to persister cells resulted in 137,000-fold more survival compared to that of addition to exponentially growing cells. Furthermore, our results seem general in that phage treatments with Klebsiella pneumonia and Pseudomonas aeruginosa also generated persister cells. Hence, along with resistant strains, bacteria also form persister cells during phage infection.