Abstract

Asia is considered an important source of influenza A virus (IAV) pandemics, owing to large, diverse viral reservoirs in poultry and swine. However, the zoonotic origins of the 2009 A/H1N1 influenza pandemic virus (pdmH1N1) remain unclear, due to conflicting evidence from swine and humans. There is strong evidence that the first human outbreak of pdmH1N1 occurred in Mexico in early 2009. However, no related swine viruses have been detected in Mexico or any part of the Americas, and to date the most closely related ancestor viruses were identified in Asian swine. Here, we use 58 new whole-genome sequences from IAVs collected in Mexican swine to establish that the swine virus responsible for the 2009 pandemic evolved in central Mexico. This finding highlights how the 2009 pandemic arose from a region not considered a pandemic risk, owing to an expansion of IAV diversity in swine resulting from long-distance live swine trade.

Article and author information

Author details

  1. Ignacio Mena

    Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Martha I Nelson

    Division of International Epidemiology and Population Studies,Fogarty International Center, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Francisco Quezada-Monroy

    Laboratorio Avi-Mex, Mexico City, Mexico
    Competing interests
    The authors declare that no competing interests exist.
  4. Jayeeta Dutta

    Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. Refugio Cortes-Fernández

    Laboratorio Avi-Mex, Mexico City, Mexico
    Competing interests
    The authors declare that no competing interests exist.
  6. J Horacio Lara-Puente

    Laboratorio Avi-Mex, Mexico City, Mexico
    Competing interests
    The authors declare that no competing interests exist.
  7. Felipa Castro-Peralta

    Laboratorio Avi-Mex, Mexico City, Mexico
    Competing interests
    The authors declare that no competing interests exist.
  8. Luis F Cunha

    Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  9. Nídia Sequeira Trovão

    Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  10. Bernardo Lozano-Dubernard

    Laboratorio Avi-Mex, Mexico City, Mexico
    Competing interests
    The authors declare that no competing interests exist.
  11. Andrew Rambaut

    Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.
  12. Harm van Bakel

    Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  13. Adolfo García-Sastre

    Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, United States
    For correspondence
    adolfo.garcia-sastre@mssm.edu
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Richard A Neher, Max Planck Institute for Developmental Biology, Germany

Version history

  1. Received: April 8, 2016
  2. Accepted: June 13, 2016
  3. Accepted Manuscript published: June 28, 2016 (version 1)
  4. Version of Record published: July 22, 2016 (version 2)

Copyright

This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

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  1. Ignacio Mena
  2. Martha I Nelson
  3. Francisco Quezada-Monroy
  4. Jayeeta Dutta
  5. Refugio Cortes-Fernández
  6. J Horacio Lara-Puente
  7. Felipa Castro-Peralta
  8. Luis F Cunha
  9. Nídia Sequeira Trovão
  10. Bernardo Lozano-Dubernard
  11. Andrew Rambaut
  12. Harm van Bakel
  13. Adolfo García-Sastre
(2016)
Origins of the 2009 H1N1 influenza pandemic in swine in Mexico
eLife 5:e16777.
https://doi.org/10.7554/eLife.16777

Share this article

https://doi.org/10.7554/eLife.16777

Further reading

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    The aim of our study was to test the hypothesis that the community contact tracing strategy of testing contacts in households immediately instead of at the end of quarantine had an impact on the transmission of SARS-CoV-2 in schools in Reggio Emilia Province.

    Methods:

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    Results:

    Median tracing delay decreased from 7 to 3.1 days and the percentage of the known infection source increased from 34–54.8% (incident rate ratio-IRR 1.61 1.40–1.86). Implementation of prompt contact tracing was associated with a 10% decrease in the number of secondary cases (excess relative risk –0.1 95% CI –0.35–0.15). Knowing the source of infection of the index case led to a decrease in secondary transmission (IRR 0.75 95% CI 0.63–0.91) while the decrease in tracing delay was associated with decreased risk of secondary cases (1/IRR 0.97 95% CI 0.94–1.01 per one day of delay). The direct effect of the intervention accounted for the 29% decrease in the number of secondary cases (excess relative risk –0.29 95%–0.61 to 0.03).

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    Prompt contact testing in the community reduces the time of contact tracing and increases the ability to identify the source of infection in school outbreaks. Although there are strong reasons for thinking it is a causal link, observed differences can be also due to differences in the force of infection and to other control measures put in place.

    Funding:

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