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

Share this article

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

Further reading

  1. DNA from 18th century teeth reveals plague secrets.

    1. Epidemiology and Global Health
    2. Microbiology and Infectious Disease
    Bo Zheng, Bronner P Gonçalves ... Caoyi Xue
    Research Article

    Background:

    In many settings, a large fraction of the population has both been vaccinated against and infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Hence, quantifying the protection provided by post-infection vaccination has become critical for policy. We aimed to estimate the protective effect against SARS-CoV-2 reinfection of an additional vaccine dose after an initial Omicron variant infection.

    Methods:

    We report a retrospective, population-based cohort study performed in Shanghai, China, using electronic databases with information on SARS-CoV-2 infections and vaccination history. We compared reinfection incidence by post-infection vaccination status in individuals initially infected during the April–May 2022 Omicron variant surge in Shanghai and who had been vaccinated before that period. Cox models were fit to estimate adjusted hazard ratios (aHRs).

    Results:

    275,896 individuals were diagnosed with real-time polymerase chain reaction-confirmed SARS-CoV-2 infection in April–May 2022; 199,312/275,896 were included in analyses on the effect of a post-infection vaccine dose. Post-infection vaccination provided protection against reinfection (aHR 0.82; 95% confidence interval 0.79–0.85). For patients who had received one, two, or three vaccine doses before their first infection, hazard ratios for the post-infection vaccination effect were 0.84 (0.76–0.93), 0.87 (0.83–0.90), and 0.96 (0.74–1.23), respectively. Post-infection vaccination within 30 and 90 days before the second Omicron wave provided different degrees of protection (in aHR): 0.51 (0.44–0.58) and 0.67 (0.61–0.74), respectively. Moreover, for all vaccine types, but to different extents, a post-infection dose given to individuals who were fully vaccinated before first infection was protective.

    Conclusions:

    In previously vaccinated and infected individuals, an additional vaccine dose provided protection against Omicron variant reinfection. These observations will inform future policy decisions on COVID-19 vaccination in China and other countries.

    Funding:

    This study was funded the Key Discipline Program of Pudong New Area Health System (PWZxk2022-25), the Development and Application of Intelligent Epidemic Surveillance and AI Analysis System (21002411400), the Shanghai Public Health System Construction (GWVI-11.2-XD08), the Shanghai Health Commission Key Disciplines (GWVI-11.1-02), the Shanghai Health Commission Clinical Research Program (20214Y0020), the Shanghai Natural Science Foundation (22ZR1414600), and the Shanghai Young Health Talents Program (2022YQ076).