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      Vibrio cholerae genomic diversity within and between patients

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          Abstract

          Cholera is a severe, water-borne diarrhoeal disease caused by toxin-producing strains of the bacterium Vibrio cholerae. Comparative genomics has revealed ‘waves’ of cholera transmission and evolution, in which clones are successively replaced over decades and centuries. However, the extent of V. cholerae genetic diversity within an epidemic or even within an individual patient is poorly understood. Here, we characterized V. cholerae genomic diversity at a micro-epidemiological level within and between individual patients from Bangladesh and Haiti. To capture within-patient diversity, we isolated multiple (8 to 20) V. cholerae colonies from each of eight patients, sequenced their genomes and identified point mutations and gene gain/loss events. We found limited but detectable diversity at the level of point mutations within hosts (zero to three single nucleotide variants within each patient), and comparatively higher gene content variation within hosts (at least one gain/loss event per patient, and up to 103 events in one patient). Much of the gene content variation appeared to be due to gain and loss of phage and plasmids within the V. cholerae population, with occasional exchanges between V. cholerae and other members of the gut microbiota. We also show that certain intra-host variants have phenotypic consequences. For example, the acquisition of a Bacteroides plasmid and non-synonymous mutations in a sensor histidine kinase gene both reduced biofilm formation, an important trait for environmental survival. Together, our results show that V. cholerae is measurably evolving within patients, with possible implications for disease outcomes and transmission dynamics.

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          Most cited references 54

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          Rates of spontaneous mutation.

          Rates of spontaneous mutation per genome as measured in the laboratory are remarkably similar within broad groups of organisms but differ strikingly among groups. Mutation rates in RNA viruses, whose genomes contain ca. 10(4) bases, are roughly 1 per genome per replication for lytic viruses and roughly 0.1 per genome per replication for retroviruses and a retrotransposon. Mutation rates in microbes with DNA-based chromosomes are close to 1/300 per genome per replication; in this group, therefore, rates per base pair vary inversely and hugely as genome sizes vary from 6 x 10(3) to 4 x 10(7) bases or base pairs. Mutation rates in higher eukaryotes are roughly 0.1-100 per genome per sexual generation but are currently indistinguishable from 1/300 per cell division per effective genome (which excludes the fraction of the genome in which most mutations are neutral). It is now possible to specify some of the evolutionary forces that shape these diverse mutation rates.
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            Comparative genomics reveals mechanism for short-term and long-term clonal transitions in pandemic Vibrio cholerae.

            Vibrio cholerae, the causative agent of cholera, is a bacterium autochthonous to the aquatic environment, and a serious public health threat. V. cholerae serogroup O1 is responsible for the previous two cholera pandemics, in which classical and El Tor biotypes were dominant in the sixth and the current seventh pandemics, respectively. Cholera researchers continually face newly emerging and reemerging pathogenic clones carrying diverse combinations of phenotypic and genotypic properties, which significantly hampered control of the disease. To elucidate evolutionary mechanisms governing genetic diversity of pandemic V. cholerae, we compared the genome sequences of 23 V. cholerae strains isolated from a variety of sources over the past 98 years. The genome-based phylogeny revealed 12 distinct V. cholerae lineages, of which one comprises both O1 classical and El Tor biotypes. All seventh pandemic clones share nearly identical gene content. Using analogy to influenza virology, we define the transition from sixth to seventh pandemic strains as a "shift" between pathogenic clones belonging to the same O1 serogroup, but from significantly different phyletic lineages. In contrast, transition among clones during the present pandemic period is characterized as a "drift" between clones, differentiated mainly by varying composition of laterally transferred genomic islands, resulting in emergence of variants, exemplified by V. cholerae O139 and V. cholerae O1 El Tor hybrid clones. Based on the comparative genomics it is concluded that V. cholerae undergoes extensive genetic recombination via lateral gene transfer, and, therefore, genome assortment, not serogroup, should be used to define pathogenic V. cholerae clones.
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              The type VI secretion system of Vibrio cholerae fosters horizontal gene transfer.

              Natural competence for transformation is a common mode of horizontal gene transfer and contributes to bacterial evolution. Transformation occurs through the uptake of external DNA and its integration into the genome. Here we show that the type VI secretion system (T6SS), which serves as a predatory killing device, is part of the competence regulon in the naturally transformable pathogen Vibrio cholerae. The T6SS-encoding gene cluster is under the positive control of the competence regulators TfoX and QstR and is induced by growth on chitinous surfaces. Live-cell imaging revealed that deliberate killing of nonimmune cells via competence-mediated induction of T6SS releases DNA and makes it accessible for horizontal gene transfer in V. cholerae.
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                Author and article information

                Journal
                Microb Genom
                Microb Genom
                MGen
                Microbial Genomics
                Microbiology Society
                2057-5858
                December 2017
                7 December 2017
                : 3
                : 12
                Affiliations
                [ 1]Department of Biological Sciences, University of Montreal , Montreal, Quebec, Canada
                [ 2]Division of Infectious Diseases, Massachusetts General Hospital , Boston, MA, USA
                [ 3]Department of Medicine, Harvard Medical School , Boston, MA, USA
                [ 4]Center for Vaccine Sciences, International Centre for Diarrhoeal Disease Research , Dhaka, Bangladesh
                [ 5]National Public Health Laboratory, Ministry of Public Health and Population , Port-au-Prince, Haiti
                [ 6]Division of Global Health Equity, Brigham and Women’s Hospital , Boston, MA, USA
                [ 7]Department of Global Health and Social Medicine, Harvard Medical School , Boston, MA, USA
                [ 8]Department of Immunology and Infectious Diseases, Harvard School of Public Health , Boston, MA, USA
                [ 9]Department of Microbiology and Immunobiology, Harvard Medical School , Boston, MA, USA
                [ 10]Department of Pediatrics, Harvard Medical School , Boston, MA, USA
                Author notes
                *Correspondence: B. Jesse Shapiro, jesse.shapiro@ 123456umontreal.ca

                All supporting data, code and protocols have been provided within the article or through supplementary data files. Supplementary material is available with the online version of this article.

                Article
                mgen000142
                10.1099/mgen.0.000142
                5761273
                29306353
                © 2017 The Authors

                This is an open access article under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

                Product
                Funding
                Funded by: Canadian Institutes of Health Research
                Funded by: Canada Research Chairs
                Funded by: National Institutes of Health
                Award ID: AI099243
                Funded by: National Institutes of Health
                Award ID: AI099243
                Funded by: National Institutes of Health
                Award ID: AI103055
                Funded by: National Institutes of Health
                Award ID: AI103055
                Funded by: National Institutes of Health
                Award ID: AI106878
                Funded by: National Institutes of Health
                Award ID: AI106878
                Funded by: National Institutes of Health
                Award ID: AI106878
                Funded by: National Institutes of Health
                Award ID: T32A1070611976
                Funded by: National Institutes of Health
                Award ID: K08AI123494
                Funded by: Robert Wood Johnson Foundation
                Categories
                Research Article
                Microbial Evolution and Epidemiology: Population Genomics
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