Targeting evolution to inhibit antibiotic resistance
Drug‐resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resist...
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| Veröffentlicht in: | The FEBS journal Jg. 287; H. 20; S. 4341 - 4353 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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England
Blackwell Publishing Ltd
01.10.2020
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| ISSN: | 1742-464X, 1742-4658, 1742-4658 |
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| Abstract | Drug‐resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an ‘optimal’ evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti‐evolution drugs from the laboratory to the clinic.
Bacteria can activate a variety of mechanisms to accelerate their access to genotypic variants, some of which can convert antibiotic‐susceptible bacteria into antibiotic‐resistant ones. These active mutagenesis mechanisms are ripe candidates for the development of anti‐evolutionary therapies, offering a novel and needed and novel approach to combating the challenge of antibiotic resistance. |
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| AbstractList | Drug‐resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an ‘optimal’ evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti‐evolution drugs from the laboratory to the clinic. Drug‐resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an ‘optimal’ evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti‐evolution drugs from the laboratory to the clinic. Bacteria can activate a variety of mechanisms to accelerate their access to genotypic variants, some of which can convert antibiotic‐susceptible bacteria into antibiotic‐resistant ones. These active mutagenesis mechanisms are ripe candidates for the development of anti‐evolutionary therapies, offering a novel and needed and novel approach to combating the challenge of antibiotic resistance. Drug resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these pro-mutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea to move from concept to execution, we first describe a set of criteria that an “optimal” evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms, and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti-evolution drugs from the laboratory to the clinic. Drug-resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an 'optimal' evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti-evolution drugs from the laboratory to the clinic.Drug-resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that are less subject to existing resistance mechanisms, history shows that this strategy by itself is unlikely to solve the problem of drug resistance. Here, we discuss inhibiting evolution as a strategy that, in combination with antibiotics, may resolve the problem. Although mutagenesis is the main driver of drug resistance development, attacking the drivers of genetic diversification in pathogens has not been well explored. Bacteria possess active mechanisms that increase the rate of mutagenesis, especially at times of stress, such as during replication within eukaryotic host cells, or exposure to antibiotics. We highlight how the existence of these promutagenic proteins (evolvability factors) presents an opportunity that can be capitalized upon for the effective inhibition of drug resistance development. To help move this idea from concept to execution, we first describe a set of criteria that an 'optimal' evolvability factor would likely have to meet to be a viable therapeutic target. We then discuss the intricacies of some of the known mutagenic mechanisms and evaluate their potential as drug targets to inhibit evolution. In principle, and as suggested by recent studies, we argue that the inhibition of these and other evolvability factors should reduce resistance development. Finally, we discuss the challenges of transitioning anti-evolution drugs from the laboratory to the clinic. |
| Author | Merrikh, Houra Kohli, Rahul M. |
| AuthorAffiliation | c Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA b Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, 37232, USA d Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA a Department of Biochemistry, Vanderbilt University, Nashville, TN, 37205, USA |
| AuthorAffiliation_xml | – name: d Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA – name: c Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA – name: a Department of Biochemistry, Vanderbilt University, Nashville, TN, 37205, USA – name: b Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, 37232, USA |
| Author_xml | – sequence: 1 givenname: Houra orcidid: 0000-0001-9956-9640 surname: Merrikh fullname: Merrikh, Houra email: houra.merrikh@vanderbilt.edu organization: Vanderbilt University Medical Center – sequence: 2 givenname: Rahul M. orcidid: 0000-0002-7689-5678 surname: Kohli fullname: Kohli, Rahul M. email: rkohli@pennmedicine.upenn.edu organization: University of Pennsylvania |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32434280$$D View this record in MEDLINE/PubMed |
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| Keywords | stress response RpoS antibiotic resistance Mfd SOS response evolution transcription-associated mutagenesis mutagenesis |
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| Snippet | Drug‐resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that... Drug-resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that... Drug resistant bacterial infections have led to a global health crisis. Although much effort is placed on the development of new antibiotics or variants that... |
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| StartPage | 4341 |
| SubjectTerms | Antibiotic resistance Antibiotics Bacterial diseases Drug development Drug resistance drugs Evolution Genetic diversity genetic variation Global health Mfd Mutagenesis mutagens Public health Resistance factors RpoS SOS response stress response Therapeutic targets therapeutics transcription‐associated mutagenesis |
| Title | Targeting evolution to inhibit antibiotic resistance |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Ffebs.15370 https://www.ncbi.nlm.nih.gov/pubmed/32434280 https://www.proquest.com/docview/2451860493 https://www.proquest.com/docview/2405334845 https://www.proquest.com/docview/2524302289 https://pubmed.ncbi.nlm.nih.gov/PMC7578009 |
| Volume | 287 |
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