Epidemiological and ecological determinants of Zika virus transmission in an urban setting

  1. José Lourenço  Is a corresponding author
  2. Maricelia Maia de Lima
  3. Nuno Rodrigues Faria
  4. Andrew Walker
  5. Moritz UG Kraemer
  6. Christian Julian Villabona-Arenas
  7. Ben Lambert
  8. Erenilde Marques de Cerqueira
  9. Oliver G Pybus
  10. Luiz CJ Alcantara
  11. Mario Recker
  1. University of Oxford, United Kingdom
  2. FIOCRUZ, Brazil
  3. Université de Montpellier, France
  4. Centre of PostGraduation in Collective Health, Universidade Estadual de Feira de Santana, Brazil
  5. University of Exeter, United Kingdom

Abstract

The Zika virus has emerged as a global public health concern. Its rapid geographic expansion is attributed to the success of Aedes mosquito vectors, but local epidemiological drivers are still poorly understood. Feira de Santana played a pivotal role in the Chikungunya epidemic in Brazil and was one of the first urban centres to report Zika infections. Using a climate-driven transmission model and notified Zika case data, we show that a low observation rate and high vectorial capacity translated into a significant attack rate during the 2015 outbreak, with a subsequent decline in 2016 and fade-out in 2017 due to herd-immunity. We find a potential Zika-related, low risk for microcephaly per pregnancy, but with significant public health impact given high attack rates. The balance between the loss of herd-immunity and viral re-importation will dictate future transmission potential of in this urban setting.

Article and author information

Author details

  1. José Lourenço

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    For correspondence
    jose.lourenco@zoo.ox.ac.uk
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-9318-2581
  2. Maricelia Maia de Lima

    Laboratory of Haematology, Genetics and Computational Biology, FIOCRUZ, Salvador, Brazil
    Competing interests
    The authors declare that no competing interests exist.
  3. Nuno Rodrigues Faria

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8839-2798
  4. Andrew Walker

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Moritz UG Kraemer

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8838-7147
  6. Christian Julian Villabona-Arenas

    Institut de Recherche pour le Développement (IRD), UMI 233, INSERM U1175, Université de Montpellier, Montpellier, France
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9928-3968
  7. Ben Lambert

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  8. Erenilde Marques de Cerqueira

    Department of Health, Centre of PostGraduation in Collective Health, Universidade Estadual de Feira de Santana, Feira de Santana, Brazil
    Competing interests
    The authors declare that no competing interests exist.
  9. Oliver G Pybus

    Department of Zoology, University of Oxford, Oxford, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  10. Luiz CJ Alcantara

    Laboratory of Haematology, Genetics and Computational Biology, FIOCRUZ, Salvador, Brazil
    Competing interests
    The authors declare that no competing interests exist.
  11. Mario Recker

    Centre for Mathematics and the Environment, University of Exeter, Penryn, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9489-1315

Funding

European Research Council (614725-PATHPHYLODYN)

  • Oliver G Pybus

Royal Society

  • Mario Recker

Wellcome Trust & Royal Society (204311/Z/16/Z)

  • Nuno Rodrigues Faria

Engineering and Physical Sciences Research Council

  • Ben Lambert

European Research Council (268904 - DIVERSITY)

  • José Lourenço
  • Andrew Walker

International Development Emerging Pandemic Threats Program-2 (AID-OAA-A-14-00102)

  • Moritz UG Kraemer

Labex EpiGenMed (ANR-10-LABX-12-01)

  • Christian Julian Villabona-Arenas

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

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

Publication history

  1. Received: June 21, 2017
  2. Accepted: September 4, 2017
  3. Accepted Manuscript published: September 9, 2017 (version 1)
  4. Version of Record published: October 12, 2017 (version 2)

Copyright

© 2017, Lourenço 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. José Lourenço
  2. Maricelia Maia de Lima
  3. Nuno Rodrigues Faria
  4. Andrew Walker
  5. Moritz UG Kraemer
  6. Christian Julian Villabona-Arenas
  7. Ben Lambert
  8. Erenilde Marques de Cerqueira
  9. Oliver G Pybus
  10. Luiz CJ Alcantara
  11. Mario Recker
(2017)
Epidemiological and ecological determinants of Zika virus transmission in an urban setting
eLife 6:e29820.
https://doi.org/10.7554/eLife.29820

Further reading

    1. Epidemiology and Global Health
    2. Microbiology and Infectious Disease
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    1. Epidemiology and Global Health
    2. Medicine
    Qing Shen, Huan Song ... Unnur Valdimarsdóttir
    Research Article Updated

    Background:

    The association between cardiovascular disease (CVD) and selected psychiatric disorders has frequently been suggested while the potential role of familial factors and comorbidities in such association has rarely been investigated.

    Methods:

    We identified 869,056 patients newly diagnosed with CVD from 1987 to 2016 in Sweden with no history of psychiatric disorders, and 910,178 full siblings of these patients as well as 10 individually age- and sex-matched unrelated population controls (N = 8,690,560). Adjusting for multiple comorbid conditions, we used flexible parametric models and Cox models to estimate the association of CVD with risk of all subsequent psychiatric disorders, comparing rates of first incident psychiatric disorder among CVD patients with rates among unaffected full siblings and population controls.

    Results:

    The median age at diagnosis was 60 years for patients with CVD and 59.2% were male. During up to 30 years of follow-up, the crude incidence rates of psychiatric disorder were 7.1, 4.6, and 4.0 per 1000 person-years for patients with CVD, their siblings and population controls. In the sibling comparison, we observed an increased risk of psychiatric disorder during the first year after CVD diagnosis (hazard ratio [HR], 2.74; 95% confidence interval [CI], 2.62–2.87) and thereafter (1.45; 95% CI, 1.42–1.48). Increased risks were observed for all types of psychiatric disorders and among all diagnoses of CVD. We observed similar associations in the population comparison. CVD patients who developed a comorbid psychiatric disorder during the first year after diagnosis were at elevated risk of subsequent CVD death compared to patients without such comorbidity (HR, 1.55; 95% CI, 1.44–1.67).

    Conclusions:

    Patients diagnosed with CVD are at an elevated risk for subsequent psychiatric disorders independent of shared familial factors and comorbid conditions. Comorbid psychiatric disorders in patients with CVD are associated with higher risk of cardiovascular mortality suggesting that surveillance and treatment of psychiatric comorbidities should be considered as an integral part of clinical management of newly diagnosed CVD patients.

    Funding:

    This work was supported by the EU Horizon 2020 Research and Innovation Action Grant (CoMorMent, grant no. 847776 to UV, PFS, and FF), Grant of Excellence, Icelandic Research Fund (grant no. 163362-051 to UV), ERC Consolidator Grant (StressGene, grant no. 726413 to UV), Swedish Research Council (grant no. D0886501 to PFS), and US NIMH R01 MH123724 (to PFS).