The DOI matches its Crossref record; 92 of the 92 references it cites were found in a registry or an index.
Persister Cells
Abstract
Persisters are dormant variants of regular cells that form stochastically in microbial populations and are highly tolerant to antibiotics. High persister (hip) mutants of Pseudomonas aeruginosa are selected in patients with cystic fibrosis. Similarly, hip mutants of Candida albicans are selected in patients with an oral thrush biofilm. These observations suggest that persisters may be the main culprit responsible for the recalcitrance of chronic infectious disease to antimicrobial therapy. Screening knockout libraries has not produced mutants lacking persisters, indicating that dormancy mechanisms are redundant. Toxin/antitoxin (TA) modules are involved in persister formation in Escherichia coli. The SOS response leads to overexpression of the TisB toxin and persister formation. TisB is a membrane-acting peptide that apparently sends cells into dormancy by decreasing the proton motive force and ATP levels. Stress responses may act as general activators of persister formation. Proteins required for maintaining persisters may represent realistic targets for discovery of drugs capable of effectively treating chronic infections.
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“Persistence is always linked to cell dormancy, a state in which the cellular metabolism temporarily ceases [111,123,124].”
From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [111]
In the citing paper
“Fungal persisters are dormant variants of wild-type cells that are tolerant to antifungal drugs, surviving high dosage of antifungals that exceed the minimal inhibitory concentration (MIC) [12,16].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [16]
In the citing paper
“It is difficult to detect persisters in planktonic cells, which is different from bacteria [12,16].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [16]
In the citing paper
“This is distinctly different from antibiotic persistence, which is mostly detected in planktonic cells [78].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [78]
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Metadata
- Authors
- Lewis, K.
- Affiliations
- Northeastern University (US)
- Corresponding author
- Lewis, Kim
- ORCID
- Lewis, Kim
- Venue
- Annual Review of Microbiology
- Publisher
- Annual Reviews
- Published
- 2010-10-13
- Volume
- 64
- Issue
- 1
- Pages
- 357-372
- ISSN
- 0066-4227 (ISSN-L)
- 1545-3251
- OpenAlex
- W4213353716
- Cited by
- 1,858
- References
- 92
- Citations by year
- 2026: 96 · 2025: 95 · 2024: 110 · 2023: 106 · 2022: 134 · 2021: 146 · 2020: 131 · 2019: 162 · 2018: 124 · 2017: 121 · 2016: 143 · 2015: 132 · 2014: 122 · 2013: 98 · 2012: 81
- FWCI
- 7.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM061162)
- National Institute of Allergy and Infectious Diseases (T-R01AO085585)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Keywords
- persister cells, antibiotic tolerance, dormancy, Pseudomonas aeruginosa, Candida albicans, cystic fibrosis, toxin-antitoxin systems, SOS response, chronic infection, antimicrobial resistance, stress response, proton motive force, therapeutic target
- MeSH terms
- Anti-Bacterial Agents, Antifungal Agents, Candida albicans, Escherichia coli, Humans, Pseudomonas aeruginosa, Drug Resistance, Bacterial, Drug Resistance, Fungal
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