1. Epidemiology and Global Health
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Nationally-representative serostudy of dengue in Bangladesh allows generalizable disease burden estimates

  1. Henrik Salje  Is a corresponding author
  2. Kishor Kumar Paul
  3. Repon Paul
  4. Isabel Rodriguez-Barraquer
  5. Ziaur Rahman
  6. Mohammad Shafiul Alam
  7. Mahmadur Rahman
  8. Hasan Mohammad Al-Amin
  9. James Heffelfinger
  10. Emily Gurley
  1. Institut Pasteur, France
  2. icddr,b, Bangladesh
  3. University of California, San Francisco, United States
  4. Institute of Epidemiology, Disease Control and Research, Bangladesh
  5. Centers for Disease Control and Prevention, United States
  6. Johns Hopkins Bloomberg School of Public Health, United States
Research Article
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Cite this article as: eLife 2019;8:e42869 doi: 10.7554/eLife.42869

Abstract

Serostudies are needed to answer generalizable questions on disease risk. However, recruitment is usually biased by age or location. We present a nationally-representative study for dengue from 70 communities in Bangladesh. We collected data on risk factors, trapped mosquitoes and tested serum for IgG. Out of 5,866 individuals, 24% had evidence of historic infection, ranging from 3% in the north to >80% in Dhaka. Being male (aOR:1.8, [95%CI:1.5-2.0]) and recent travel (aOR:1.3, [1.1-1.8]) were linked to seropositivity. Using catalytic models, we estimate that 40 million [34.3-47.2] people have been infected with 2.4 million ([1.3-4.5]) annual infections. Had we visited only 20 communities, seropositivity estimates would have ranged from 13% to 37%, highlighting the lack of representativeness generated by small numbers of communities. Our findings have implications for both the design of serosurveys and tackling dengue in Bangladesh.

Data availability

All data generated or analysed during this study are included in the manuscript and supporting files with the exception of precise coordinate information of households.

Article and author information

Author details

  1. Henrik Salje

    Mathematical Modelling of Infectious Diseases, Institut Pasteur, Paris, France
    For correspondence
    hsalje@pasteur.fr
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-3626-4254
  2. Kishor Kumar Paul

    Program for Emerging Infections, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6054-3571
  3. Repon Paul

    Program for Emerging Infections, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
  4. Isabel Rodriguez-Barraquer

    Department of Medicine, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-6784-1021
  5. Ziaur Rahman

    Program for Emerging Infections, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
  6. Mohammad Shafiul Alam

    Program for Emerging Infections, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
  7. Mahmadur Rahman

    Institute of Epidemiology, Disease Control and Research, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
  8. Hasan Mohammad Al-Amin

    Program for Emerging Infections, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
    Competing interests
    The authors declare that no competing interests exist.
  9. James Heffelfinger

    Division of Global Health Protection, Centers for Disease Control and Prevention, Atlanta, United States
    Competing interests
    The authors declare that no competing interests exist.
  10. Emily Gurley

    Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-8648-9403

Funding

Centers for Disease Control and Prevention

  • Henrik Salje
  • Emily Gurley

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

Ethics

Human subjects: This study was approved by the icddr,b ethical review board. (protocol number PR-14058). The U.S. Centers for Disease Control and Prevention relied on icddr,b's ethical review board approval. All adult participants provided written, informed consent after receiving detailed explanation of the study and procedures. Parents/guardians of all child participants were asked to provide written, informed consent on their behalf.

Reviewing Editor

  1. Ben Cooper, Mahidol Oxford Tropical Medicine Research Unit, Thailand

Publication history

  1. Received: October 15, 2018
  2. Accepted: April 4, 2019
  3. Accepted Manuscript published: April 8, 2019 (version 1)
  4. Version of Record published: May 13, 2019 (version 2)
  5. Version of Record updated: May 16, 2019 (version 3)

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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Further reading

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    Morgan P Kain et al.
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    Identifying the key vector and host species that drive the transmission of zoonotic pathogens is notoriously difficult but critical for disease control. We present a nested approach for quantifying the importance of host and vectors that integrates species’ physiological competence with their ecological traits. We apply this framework to a medically important arbovirus, Ross River virus (RRV), in Brisbane, Australia. We find that vertebrate hosts with high physiological competence are not the most important for community transmission; interactions between hosts and vectors largely underpin the importance of host species. For vectors, physiological competence is highly important. Our results identify primary and secondary vectors of RRV and suggest two potential transmission cycles in Brisbane: an enzootic cycle involving birds and an urban cycle involving humans. The framework accounts for uncertainty from each fitted statistical model in estimates of species’ contributions to transmission and has has direct application to other zoonotic pathogens.

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    2. Genetics and Genomics
    Mohd Anisul et al.
    Research Article Updated

    Background:

    The virus SARS-CoV-2 can exploit biological vulnerabilities (e.g. host proteins) in susceptible hosts that predispose to the development of severe COVID-19.

    Methods:

    To identify host proteins that may contribute to the risk of severe COVID-19, we undertook proteome-wide genetic colocalisation tests, and polygenic (pan) and cis-Mendelian randomisation analyses leveraging publicly available protein and COVID-19 datasets.

    Results:

    Our analytic approach identified several known targets (e.g. ABO, OAS1), but also nominated new proteins such as soluble Fas (colocalisation probability >0.9, p=1 × 10-4), implicating Fas-mediated apoptosis as a potential target for COVID-19 risk. The polygenic (pan) and cis-Mendelian randomisation analyses showed consistent associations of genetically predicted ABO protein with several COVID-19 phenotypes. The ABO signal is highly pleiotropic, and a look-up of proteins associated with the ABO signal revealed that the strongest association was with soluble CD209. We demonstrated experimentally that CD209 directly interacts with the spike protein of SARS-CoV-2, suggesting a mechanism that could explain the ABO association with COVID-19.

    Conclusions:

    Our work provides a prioritised list of host targets potentially exploited by SARS-CoV-2 and is a precursor for further research on CD209 and FAS as therapeutically tractable targets for COVID-19.

    Funding:

    MAK, JSc, JH, AB, DO, MC, EMM, MG, ID were funded by Open Targets. J.Z. and T.R.G were funded by the UK Medical Research Council Integrative Epidemiology Unit (MC_UU_00011/4). JSh and GJW were funded by the Wellcome Trust Grant 206194. This research was funded in part by the Wellcome Trust [Grant 206194]. For the purpose of open access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission.