ReviewCell host & microbe2024
Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.
Review in Cell host & microbe, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed.
- Simulating the host niche: balancing complexity and control in the experimental evolution of antibiotic resistance and pathoadaptation.Microbiology (Reading, England) · 2026Review
- Contributions of persisters and the Eagle effect to survival ofMicrobiology spectrum · 2026Article
- Reply to Gong et al.: Antibiotic tolerance coupled with limited benefit from drainage: Clinical challenges inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Stress History Establishes a Transient Tolerant State That Shapes Antibiotic Survival Upon Resuscitation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Trehalose-Based Phenotypic Screen Identifies Candidate Inhibitors ofAntibiotics (Basel, Switzerland) · 2026Article
- Fast-growing intracellular Mycobacterium tuberculosis populations evade antibiotic treatment.Nature communications · 2026Article
- Restoring Microbial Signaling: A Metabolite-Immune-Redox Framework for Postbiotic Host-Directed Interventions.Medical sciences (Basel, Switzerland) · 2026Review
- The Pharmacology of Bacterial Persistence: From Antibiotic Tolerance to Antimicrobial Resistance.Antibiotics (Basel, Switzerland) · 2026Review
- Heterogeneity in microbial antibiotic responses: genetic basis and within-host evolution.Trends in genetics : TIG · 2026Review
- Single-cell heterogeneity in ribosome levels and protein synthesis during nutrient starvation is driven by cAMP signaling.Science advances · 2026Article
- Growth arrest of Mycobacterium tuberculosis in acidic environments enhances their survival of antibiotic treatment.PLoS biology · 2026Article
- Bacterial Persister Cells as Evolutionary Catalysts of Antibiotic Resistance: Mechanisms, Clinical Implications, and Therapeutic Strategies.Antibiotics (Basel, Switzerland) · 2026Review
- Article
- Review
- Integrating chemical, genetic, and feasibility assessments for anti-tubercular target validation.EMBO molecular medicine · 2026Review
- Expression patterns of core metabolic genes and elevated intracellular ROS confer drug tolerance inMicrobiology spectrum · 2026Article
- Granulomas microenvironment-guided sono-immunotherapy to treat and prevent recurrence of tuberculosis.Nature communications · 2026Article
- A two-step screen identifies a small molecule that disrupts membrane voltage and is effective against growing and persister gram-negative bacteria.Microbiology spectrum · 2026Article
- Parallel Genome-Wide CRISPR Screens Reveal SORL1 and ZFYVE19 as Sequential Host Determinants of Salmonella Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Methicillin-resistant and susceptible Staphylococcus aureus: tolerance, immune evasion and treatment.Nature reviews. Microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Antibiotic resistance, typically associated with genetic changes within a bacterial population, is a frequent contributor to antibiotic treatment failures. Antibiotic persistence and tolerance, which we collectively term recalcitrance, represent transient phenotypic changes in the bacterial population that prolong survival in the presence of typically lethal concentrations of antibiotics. Antibiotic recalcitrance is challenging to detect and investigate-traditionally studied under in vitro conditions, our understanding during infection and its contribution to antibiotic failure is limited. Recently, significant progress has been made in the study of antibiotic-recalcitrant populations in pathogenic species, including Mycobacterium tuberculosis, Staphylococcus aureus, Salmonella enterica, and Yersiniae, in the context of the host environment. Despite the diversity of these pathogens and infection models, shared signals and responses promote recalcitrance, and common features and vulnerabilities of persisters and tolerant bacteria have emerged. These will be discussed here, along with progress toward developing therapeutic interventions to better treat recalcitrant pathogens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.