Publications by authors named "Kalen M Hall"
Article Synopsis
- Pseudomonas aeruginosa, when losing DNA mismatch repair (MMR), becomes a hypermutator, leading to high rates of multidrug resistance (MDR), especially after exposure to antibiotics.
- Hypermutated MMR-deficient P. aeruginosa has a specific mutational signature and quickly develops MDR through shared resistance mechanisms across different drug classes.
- Analyzing mutational signatures of P. aeruginosa in patients shows many MMR-deficient strains are already MDR or likely to become resistant, indicating that this analysis could be a valuable diagnostic tool for predicting and managing MDR in clinical settings.
Here, we describe the continued synthetic molecular evolution of a lineage of host-compatible antimicrobial peptides (AMP) intended for the treatment of wounds infected with drug-resistant, biofilm-forming bacteria. The peptides tested are variants of an evolved AMP called d-amino acid CONsensus with Glycine Absent (d-CONGA), which has excellent antimicrobial activities and . In this newest generation of rational d-CONGA variants, we tested multiple sequence-structure-function hypotheses that had not been tested in previous generations.
View Article and Find Full Text PDFThe role of the hypermutator phenotype on the shift from acute to chronic virulence during respiratory infection.
Front Cell Infect Microbiol
August 2022
Chronic respiratory infection (CRI) with (Pa) presents many unique challenges that complicate treatment. One notable challenge is the hypermutator phenotype which is present in up to 60% of sampled CRI patient isolates. Hypermutation can be caused by deactivating mutations in DNA mismatch repair (MMR) genes including , , and .
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