Molecular mechanisms driving the antagonistic coevolution of viral satellites and bacteriophages in Vibrio cholerae
霍乱弧菌病毒卫星和噬菌体拮抗协同进化的分子机制
基本信息
- 批准号:10033684
- 负责人:
- 金额:$ 61.28万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2020
- 资助国家:美国
- 起止时间:2020-06-01 至 2025-05-31
- 项目状态:未结题
- 来源:
- 关键词:AddressAutomobile DrivingBackBacterial Antibiotic ResistanceBacteriophagesBangladeshBiochemicalBiological AssayBiological ModelsCause of DeathCholeraCollectionConflict (Psychology)DangerousnessDepressed moodDevelopmentDiseaseDysenteryElementsEpidemicEvolutionExtinction (Psychology)GeneticGenetic RecombinationGenomeGenomic InstabilityGenomicsGenotypeGeographyGoalsHumanIn VitroIncidenceInfectionInfection ControlIntegraseIntestinesIslandKnowledgeLaboratoriesLeftLifeLinkMeasuresMediatingMobile Genetic ElementsMolecularMonitorNatural DisastersOrganismParasitesPatientsPatternPopulationPositioning AttributePredatory BehaviorPredispositionProductionPublic HealthRaceReplication OriginResourcesRoleShapesSourceStudy modelsSystemTestingTherapeuticTherapeutic community techniqueTimeVariantVibrio choleraeViralVirusWorkarmdiarrheal diseasedriving forcehuman diseasein vivoinsightmicrobialnovelnucleasepandemic diseasepathogenpathogenic bacteriaprophylacticsocioeconomicsstool sampletransmission process
项目摘要
Illness and death caused by infectious diarrheal disease agents, like Vibrio cholerae, are major threats to
public health and significant barriers to socioeconomic development worldwide. Natural disasters and
continuing conflict in some depressed regions threaten to exacerbate the already rising incidence of cholera
globally. As the focus of several elegant studies documenting genomic changes in epidemic strains over the
last century, V. cholerae has become a well-studied model for pathogen evolution. Despite this, the
mechanisms and driving forces underlying historical and current changes are not yet understood. The arms
race between viruses and their host organisms is a key driving force in the evolution of all cellular life. Indeed
V. cholerae must defend against the ubiquitous threat of predatory phages in aquatic reservoirs and in the
intestinal tract during disease in humans. Our laboratory has shown that V. cholerae has evolved to use PLEs
to defend against the predominant predatory phage ICP1. PLEs are parasitic mobile genetic elements that
completely abolish ICP1 production while exploiting phage resources to further their own spread. Therefore,
PLEs can be viewed both as defense systems for V. cholerae, and as phage satellites that exploit ICP1 for
their own mobilization. A significant hallmark of V. cholerae PLEs is that previously prevalent PLEs disappear
globally when new variants emerge, indicating that each variant is selected by unknown factors over time.
However, we do not understand why such changes occur, and how new variants come to dominate over earlier
prevalent variants. We hypothesize that antagonism with ICP1 and other mobile genetic elements in V.
cholerae has driven the successive evolution of PLEs. We also hypothesize that reciprocal adaptations in PLE
to counter those attacks have contributed to the hallmark pattern of variant extinction and replacement. To
dissect the mechanisms of successive evolution of PLEs we will pursue the following specific aims: 1) We will
determine how ICP1 antagonism selected for PLE variants with alternative replication modules. 2) We will
define how PLE 2 mobilization renders it susceptible to ICP1 antagonism. 3) We will determine how an
interfering defense island antagonizes ICP1 and PLE activity. 4) We will investigate PLE-PLE competition and
the potential for recombination as a driver of PLE evolution. The proposed studies will provide insight into how
epidemic V. cholerae is selected for over time and will aid in tracking the dissemination of epidemic strains.
This knowledge will further enhance our understanding of phage-mediated perturbations to microbial
populations in healthy and diseased states, and advance our ability to manipulate these communities for
therapeutic or prophylactic benefit.
由霍乱弧菌等传染性腹泻病原体引起的疾病和死亡是对人类健康的主要威胁
项目成果
期刊论文数量(0)
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Kimberley Diane Seed其他文献
Kimberley Diane Seed的其他文献
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{{ truncateString('Kimberley Diane Seed', 18)}}的其他基金
Molecular mechanisms driving the antagonistic coevolution of viral satellites and bacteriophages in Vibrio cholerae
霍乱弧菌病毒卫星和噬菌体拮抗协同进化的分子机制
- 批准号:
10401451 - 财政年份:2020
- 资助金额:
$ 61.28万 - 项目类别:
Molecular mechanisms driving the antagonistic coevolution of viral satellites and bacteriophages in Vibrio cholerae
霍乱弧菌病毒卫星和噬菌体拮抗协同进化的分子机制
- 批准号:
10176401 - 财政年份:2020
- 资助金额:
$ 61.28万 - 项目类别:
Molecular mechanisms driving the antagonistic coevolution of viral satellites and bacteriophages in Vibrio cholerae
霍乱弧菌病毒卫星和噬菌体拮抗协同进化的分子机制
- 批准号:
10624961 - 财政年份:2020
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
9795616 - 财政年份:2018
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
10366735 - 财政年份:2016
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
9754762 - 财政年份:2016
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
10494121 - 财政年份:2016
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
10682489 - 财政年份:2016
- 资助金额:
$ 61.28万 - 项目类别:
Phage resistance and mobile genetic elements in Vibrio cholerae
霍乱弧菌的噬菌体抗性和移动遗传元件
- 批准号:
9360091 - 财政年份:2016
- 资助金额:
$ 61.28万 - 项目类别:
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