ArticleMicrobial biotechnology2024
Phages produce persisters.
Article in Microbial biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Phenotypic heterogeneity and genetic mechanisms of phage resistance in hypervirulent carbapenem-resistantVirulence · 2026Article
- Seeing Bacterial Persistence Through Different Experimental Lenses: How Methodology Shapes Biological Interpretation.Pathogens (Basel, Switzerland) · 2026Review
- PMI TechNote: Bacteriophages-From the Petri Dish to Conquering the Nooks and Crannies of Difficult-to-Treat Infections.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026Review
- Bacterial immune systems.Antonie van Leeuwenhoek · 2026Review
- Ribosome State Distributions Define Escherichia coli Persister Physiology: Links to Formation, Stress Responses, and Resuscitation Dynamics.Microbial biotechnology · 2026Article
- Phase variation inEngineering microbiology · 2026Article
- Phage-Based Approaches to ChronicAntibiotics (Basel, Switzerland) · 2026Review
- Phage infection fronts trigger early sporulation and viral entrapment in bacterial populations.The ISME journal · 2026Article
- Persister cells form based on low ribosome content inSustainable microbiology · 2026Article
- Antibiotic Persister Cells in Acinetobacter baumannii: Overview of Molecular Mechanisms and Removal Strategies.Environmental microbiology · 2025Review
- Adsorption of phage T2 is inhibited due to inversion of cryptic prophage DNA by the serine recombinase PinQ.Nucleic acids research · 2025Article
- Investigating the phenotypic alterations associated with hypermucoviscous hypervirulent Klebsiella pneumoniae during phage resistance development.BMC microbiology · 2025Article
- Heat stress induces phage tolerance ineLife · 2025Article
- Phage therapy for Klebsiella pneumoniae: Understanding bacteria-phage interactions for therapeutic innovations.PLoS pathogens · 2025Review
- Microbial community structure is affected by phage-resistance associated increases in host density.FEMS microbiology ecology · 2025Article
- Harnessing Bacteriophages for Sustainable Crop Protection in the Face of Climate Change.Microbial biotechnology · 2025Review
- Efficacy of a commercial bacteriophage cocktail against planktonic cells and both thin and thick biofilms of skin pathogens, measured using isothermal microcalorimetry.Frontiers in microbiology · 2025Article
- Microbes Saving Lives and Reducing Suffering.Microbial biotechnology · 2025Article
- Conformational change as a mechanism for toxin activation in bacterial toxin-antitoxin systems.Journal of virology · 2024Review
- Phage biocontrol success of bacterial wilt depends on synergistic interactions with resident rhizosphere microbiota.Microbial biotechnology · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
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.
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