Eighteenth century Yersinia pestis genomes reveal the long-term persistence of an historical plague focus

  1. Kirsten I Bos
  2. Alexander Herbig
  3. Jason Sahl
  4. Nicholas Waglechner
  5. Mathieu Fourment
  6. Stephen A Forrest
  7. Jennifer Klunk
  8. Verena J Schuenemann
  9. Debi Poinar
  10. Melanie Kuch
  11. G Brian Golding
  12. Olivier Dutour
  13. Paul Keim
  14. David M Wagner
  15. Edward C Holmes
  16. Johannes Krause  Is a corresponding author
  17. Hendrik N Poinar
  1. University of Tübingen, Germany
  2. Northern Arizona University, United States
  3. McMaster University, Canada
  4. The University of Sydney, Australia
  5. Université Bordeaux, France

Abstract

The 14th-18th century pandemic of Yersinia pestis caused devastating disease outbreaks in Europe for almost 400 years. The reasons for plague's persistence and abrupt disappearance in Europe are poorly understood, but could have been due to either the presence of now-extinct plague foci in Europe itself, or successive disease introductions from other locations. Here we present five Y. pestis genomes from one of the last European outbreaks of plague, from 1722 in Marseille, France. The lineage identified has not been found in any extant Y. pestis foci sampled to date, and has its ancestry in strains obtained from victims of the 14th century Black Death. These data suggest the existence of a previously uncharacterized historical plague focus that persisted for at least three centuries. We propose that this disease source may have been responsible for the many resurgences of plague in Europe following the Black Death.

Article and author information

Author details

  1. Kirsten I Bos

    Department of Archeological Sciences, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  2. Alexander Herbig

    Department of Archeological Sciences, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  3. Jason Sahl

    Center for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Nicholas Waglechner

    Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.
  5. Mathieu Fourment

    Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Life and Environmental Sciences and Sydney Medical School, The University of Sydney, Sydney, Australia
    Competing interests
    The authors declare that no competing interests exist.
  6. Stephen A Forrest

    Department of Archeological Sciences, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  7. Jennifer Klunk

    McMaster Ancient DNA Centre, Department of Anthropology, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.
  8. Verena J Schuenemann

    Department of Archeological Sciences, University of Tübingen, Tübingen, Germany
    Competing interests
    The authors declare that no competing interests exist.
  9. Debi Poinar

    McMaster Ancient DNA Centre, Department of Anthropology, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.
  10. Melanie Kuch

    McMaster Ancient DNA Centre, Department of Anthropology, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.
  11. G Brian Golding

    Department of Biology, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.
  12. Olivier Dutour

    Laboratoire d'anthropologie biologique Paul Broca, Ecole Pratique des Hautes Etudes, PACEA, Université Bordeaux, Bordeaux, France
    Competing interests
    The authors declare that no competing interests exist.
  13. Paul Keim

    Center for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, United States
    Competing interests
    The authors declare that no competing interests exist.
  14. David M Wagner

    Center for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, United States
    Competing interests
    The authors declare that no competing interests exist.
  15. Edward C Holmes

    Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Life and Environmental Sciences and Sydney Medical School, The University of Sydney, Sydney, Australia
    Competing interests
    The authors declare that no competing interests exist.
  16. Johannes Krause

    Department of Archeological Sciences, University of Tübingen, Tübingen, Germany
    For correspondence
    johannes.krause@uni-tuebingen.de
    Competing interests
    The authors declare that no competing interests exist.
  17. Hendrik N Poinar

    Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Canada
    Competing interests
    The authors declare that no competing interests exist.

Copyright

© 2016, Bos et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Kirsten I Bos
  2. Alexander Herbig
  3. Jason Sahl
  4. Nicholas Waglechner
  5. Mathieu Fourment
  6. Stephen A Forrest
  7. Jennifer Klunk
  8. Verena J Schuenemann
  9. Debi Poinar
  10. Melanie Kuch
  11. G Brian Golding
  12. Olivier Dutour
  13. Paul Keim
  14. David M Wagner
  15. Edward C Holmes
  16. Johannes Krause
  17. Hendrik N Poinar
(2016)
Eighteenth century Yersinia pestis genomes reveal the long-term persistence of an historical plague focus
eLife 5:e12994.
https://doi.org/10.7554/eLife.12994

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https://doi.org/10.7554/eLife.12994

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    1. Epidemiology and Global Health
    Yuan Zhang, Dan Tang ... Xing Zhao
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    Biological aging exhibits heterogeneity across multi-organ systems. However, it remains unclear how is lifestyle associated with overall and organ-specific aging and which factors contribute most in Southwest China.

    Methods:

    This study involved 8396 participants who completed two surveys from the China Multi-Ethnic Cohort (CMEC) study. The healthy lifestyle index (HLI) was developed using five lifestyle factors: smoking, alcohol, diet, exercise, and sleep. The comprehensive and organ-specific biological ages (BAs) were calculated using the Klemera–Doubal method based on longitudinal clinical laboratory measurements, and validation were conducted to select BA reflecting related diseases. Fixed effects model was used to examine the associations between HLI or its components and the acceleration of validated BAs. We further evaluated the relative contribution of lifestyle components to comprehension and organ systems BAs using quantile G-computation.

    Results:

    About two-thirds of participants changed HLI scores between surveys. After validation, three organ-specific BAs (the cardiopulmonary, metabolic, and liver BAs) were identified as reflective of specific diseases and included in further analyses with the comprehensive BA. The health alterations in HLI showed a protective association with the acceleration of all BAs, with a mean shift of –0.19 (95% CI −0.34, –0.03) in the comprehensive BA acceleration. Diet and smoking were the major contributors to overall negative associations of five lifestyle factors, with the comprehensive BA and metabolic BA accounting for 24% and 55% respectively.

    Conclusions:

    Healthy lifestyle changes were inversely related to comprehensive and organ-specific biological aging in Southwest China, with diet and smoking contributing most to comprehensive and metabolic BA separately. Our findings highlight the potential of lifestyle interventions to decelerate aging and identify intervention targets to limit organ-specific aging in less-developed regions.

    Funding:

    This work was primarily supported by the National Natural Science Foundation of China (Grant No. 82273740) and Sichuan Science and Technology Program (Natural Science Foundation of Sichuan Province, Grant No. 2024NSFSC0552). The CMEC study was funded by the National Key Research and Development Program of China (Grant No. 2017YFC0907305, 2017YFC0907300). The sponsors had no role in the design, analysis, interpretation, or writing of this article.