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Infect Immun. 2020 Feb 24. pii: IAI.00926-19. doi: 10.1128/IAI.00926-19. [Epub ahead of print]

Fitness trade-offs resulting from bacteriophage resistance potentiate synergistic antibacterial strategies.

Author information

1
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
2
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, 80045, USA. breck.duerkop@cuanschutz.edu.

Abstract

Bacteria that cause life-threatening infections in humans are becoming increasingly difficult to treat. In some instances, this is due to intrinsic and acquired antibiotic resistance, indicating that new therapeutic approaches are needed to combat bacterial pathogens. There is renewed interest in utilizing viruses of bacteria known as bacteriophages (phages) as potential antibacterial therapeutics. However, critics suggest that similar to antibiotics, the development of phage resistant bacteria will halt clinical phage therapy. Although the emergence of phage resistant bacteria is likely inevitable, there is a growing body of literature showing that phage selective pressure promotes mutations in bacteria that allow them to subvert phage infection, but with a cost to their fitness. Such fitness trade-offs include reduced virulence, resensitization to antibiotics and colonization defects. Resistance to phage nucleic acid entry, primarily via cell surface modifications, compromises bacterial fitness during antibiotic and host immune system pressure. In this Mini Review we will explore the mechanisms behind phage resistance in bacterial pathogens and the physiological consequences of acquiring phage resistance phenotypes. With this knowledge, it may be possible to use phages to alter bacterial populations making them more tractable to current therapeutic strategies.

PMID:
32094257
DOI:
10.1128/IAI.00926-19
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