1. Epidemiology and Global Health
  2. Microbiology and Infectious Disease
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Mapping global environmental suitability for Zika virus

  1. Jane P Messina  Is a corresponding author
  2. Moritz UG Kraemer
  3. Oliver J Brady
  4. David M Pigott
  5. Freya M Shearer
  6. Daniel J Weiss
  7. Nick Golding
  8. Corrine W Ruktanonchai
  9. Peter W Gething
  10. Emily Cohn
  11. John S Brownstein
  12. Kamran Khan
  13. Andrew J Tatem
  14. Thomas Jaenisch
  15. Christopher JL Murray
  16. Fatima Marinho
  17. Thomas W Scott
  18. Simon I Hay
  1. University of Oxford, United Kingdom
  2. University of Melbourne, United Kingdom
  3. University of Southampton, United Kingdom
  4. Harvard Medical School, United Kingdom
  5. Harvard Medical School, United States
  6. University of Toronto, Canada
  7. Heidelberg University Hospital, Germany
  8. University of Washington, Seattle, United States
  9. Ministry of Health Brazil, Brazil
  10. University of California Davis, United States
Research Article
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Cite this article as: eLife 2016;5:e15272 doi: 10.7554/eLife.15272
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Abstract

Zika virus was discovered in Uganda in 1947 and is transmitted by Aedes mosquitoes, which also act as vectors for dengue and chikungunya viruses throughout much of the tropical world. In 2007, an outbreak in the Federated States of Micronesia sparked public health concern. In 2013, the virus began to spread across other parts of Oceania and in 2015, a large outbreak in Latin America began in Brazil. Possible associations with microcephaly and Guillain-Barré syndrome observed in this outbreak have raised concerns about continued global spread of Zika virus, prompting its declaration as a Public Health Emergency of International Concern by the World Health Organization. We conducted species distribution modelling to map environmental suitability for Zika. We show a large portion of tropical and sub-tropical regions globally have suitable environmental conditions with over 2.17 billion people inhabiting these areas.

Article and author information

Author details

  1. Jane P Messina

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    For correspondence
    jane.messina@zoo.ox.ac.uk
    Competing interests
    No competing interests declared.

  2. Moritz UG Kraemer

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  3. Oliver J Brady

    Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  4. David M Pigott

    Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  5. Freya M Shearer

    Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  6. Daniel J Weiss

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  7. Nick Golding

    Department of BioSciences, University of Melbourne, Parkville, United Kingdom
    Competing interests
    No competing interests declared.

  8. Corrine W Ruktanonchai

    WorldPop project, Department of Geography and Environment, University of Southampton, Southampton, United Kingdom
    Competing interests
    No competing interests declared.

  9. Peter W Gething

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    No competing interests declared.

  10. Emily Cohn

    Boston Children's Hospital, Harvard Medical School, Boston, United Kingdom
    Competing interests
    No competing interests declared.

  11. John S Brownstein

    Department of Pediatrics, Harvard Medical School, Boston, United States
    Competing interests
    No competing interests declared.

  12. Kamran Khan

    Department of Medicine, Division of Infectious Diseases, University of Toronto, Toronto, Canada
    Competing interests
    No competing interests declared.

  13. Andrew J Tatem

    WorldPop project, Department of Geography and Environment, University of Southampton, Southampton, United Kingdom
    Competing interests
    No competing interests declared.

  14. Thomas Jaenisch

    Section Clinical Tropical Medicine, Department for Infectious Diseases, Heidelberg University Hospital, Heidelberg, Germany
    Competing interests
    No competing interests declared.

  15. Christopher JL Murray

    Institute for Health Metrics and Evaluation, University of Washington, Seattle, Seattle, United States
    Competing interests
    No competing interests declared.

  16. Fatima Marinho

    Secretariat of Health Surveillance, Ministry of Health Brazil, Brasilia, Brazil
    Competing interests
    No competing interests declared.

  17. Thomas W Scott

    Department of Entomology and Nematology, University of California Davis, Davis, United States
    Competing interests
    No competing interests declared.

  18. Simon I Hay

    Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
    Competing interests
    Simon I Hay, Reviewing editor; eLife.

Reviewing Editor

  1. Mark Jit, London School of Hygiene & Tropical Medicine, and Public Health England, United Kingdom

Publication history

  1. Received: February 15, 2016
  2. Accepted: April 10, 2016
  3. Accepted Manuscript published: April 19, 2016 (version 1)
  4. Version of Record published: June 1, 2016 (version 2)

Copyright

© 2016, Messina 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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    Biomarkers of low-grade inflammation have been associated with susceptibility to a severe infectious disease course, even when measured prior to disease onset. We investigated whether metabolic biomarkers measured by nuclear magnetic resonance (NMR) spectroscopy could be associated with susceptibility to severe pneumonia (2507 hospitalised or fatal cases) and severe COVID-19 (652 hospitalised cases) in 105,146 generally healthy individuals from UK Biobank, with blood samples collected 2007–2010. The overall signature of metabolic biomarker associations was similar for the risk of severe pneumonia and severe COVID-19. A multi-biomarker score, comprised of 25 proteins, fatty acids, amino acids and lipids, was associated equally strongly with enhanced susceptibility to severe COVID-19 (odds ratio 2.9 [95%CI 2.1–3.8] for highest vs lowest quintile) and severe pneumonia events occurring 7–11 years after blood sampling (2.6 [1.7–3.9]). However, the risk for severe pneumonia occurring during the first 2 years after blood sampling for people with elevated levels of the multi-biomarker score was over four times higher than for long-term risk (8.0 [4.1–15.6]). If these hypothesis generating findings on increased susceptibility to severe pneumonia during the first few years after blood sampling extend to severe COVID-19, metabolic biomarker profiling could potentially complement existing tools for identifying individuals at high risk. These results provide novel molecular understanding on how metabolic biomarkers reflect the susceptibility to severe COVID-19 and other infections in the general population.