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Whole Genome Sequencing / Acinetobacter Infections / Crispr-cas Systems · Journal article
Virulence · July 28, 2026
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This study describes isolation and characterization of a novel Acinetobacter baumannii myovirus, identifies galE insertional mutation as the primary resistance mechanism, and demonstrates that capsule loss attenuates virulence in an invertebrate infection model while enhancing biofilm formation. The work is mechanistically sound but remains preclinical and limited to a single bacterial isolate with no human clinical translation.
Experimental microbiology study with genomic, transcriptomic, and functional validation. Acinetobacter baumannii isolate harboring I-F CRISPR-Cas system; phage-resistant mutants derived from this isolate.. Intervention: Novel myovirus (stable at 40–50°C); combination phage with carbenicillin or ceftazidime.. Compared with: Wild-type A. baumannii isolate; phage-resistant mutants (ΔgalE); antibiotic or phage monotherapy..
Novel myovirus isolated and confirmed to be stable at 40–50°C and distinct from published phages by whole-genome analysis. Primary phage resistance mechanism: insertional mutation in galE (UDP-glucose 4-epimerase) causing capsule loss, validated by targeted gene knockout. ΔgalE mutants demonstrated significantly reduced lethality in Galleria mellonella infection model and enhanced susceptibility to serum killing.
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These findings suggest a novel phage with potential therapeutic value and reveal that phage-induced resistance mutations may paradoxically reduce bacterial virulence—a mechanism worth exploring in combination therapy strategies. However, all results remain in vitro or in invertebrate models and require validation in mammalian infection systems before clinical consideration.
Single-isolate laboratory study characterizing a novel phage and resistance mechanisms with in vitro and insect model validation, but lacking human clinical data or comparative efficacy trials.
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These findings suggest a novel phage with potential therapeutic value and reveal that phage-induced resistance mutations may paradoxically reduce bacterial virulence—a mechanism worth exploring in combination therapy strategies. However, all results remain in vitro or in invertebrate models and require validation in mammalian infection systems before clinical consideration.
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Phage therapy represents a promising alternative for combating bacterial infections. This study employed an A. baumannii isolate harboring the I-F CRISPR-Cas system as a host to isolate phage and evaluate its biological characteristics. Phage-resistant mutants were screened using a double-layer agar plate assay, and the underlying molecular mechanisms were identified through whole-genome sequencing, followed by validation via gene knockout. Transcriptome sequencing was subsequently applied to alterations in the global regulatory networks of these mutants. Our results demonstrate the successful isolation of a novel myovirus, stable at 40-50°C, which was successfully isolated and found to utilize the capsule as its adsorption receptor. Whole-genomic analysis confirmed its distinction from currently published phages. Investigation into the primary resistance mechanism revealed that the capsule loss, due to an insertional mutation in the UDP-glucose 4-epimerase encoding gene galE. This conclusion was further validated through targeted gene knockout of galE. This defect concurrently attenuated bacterial virulence, as demonstrated by significantly reduced lethality in the Galleria mellonella infection model and enhanced susceptibility to serum killing, while concurrently enhancing the capacity for biofilm formation. Transcriptomic profiling indicated that the ΔgalE significantly upregulated multiple biofilm-associated genes and remodeled the transcriptomic-wide regulatory. Furthermore, the combination of carbenicillin or ceftazidime with the phage exhibited a synergistic effect in vitro, effectively inhibiting biofilm formation and suppressing the emergence of phage resistance. Overall, this work characterizes a novel phage and delineates the host's biological network changes triggered by phage resistance, offering valuable insights for developing phage-based antimicrobial strategies.
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