Serological evidence of zoonotic filovirus exposure among bushmeat hunters in Guinea

Joseph Akoi Boré, Joseph W. S. Timothy, Tom Tipton, Ifono Kekoura, Yper Hall, Grace Hood, Stephanie Longet, Kimberly Fornace, Millimono S. Lucien, Sarah Katarina Fehling, Beatrice K. Koivogui, Si’Ana A. Coggins, Eric D. Laing, Christopher C. Broder, Faly Magassouba N’, Thomas Strecker, Jeremy Rossman, Kader Konde and Miles W. Carroll ()
Additional contact information
Joseph Akoi Boré: Ministère de la Santé et de l’hygiène publique
Joseph W. S. Timothy: London School of Hygiene Tropical Medicine
Tom Tipton: University of Oxford
Ifono Kekoura: Ministère de la Santé et de l’hygiène publique
Yper Hall: UK Health Security Agency
Grace Hood: University of Oxford
Stephanie Longet: University of Oxford
Kimberly Fornace: National University of Singapore
Millimono S. Lucien: Ministère de la Santé et de l’hygiène publique
Sarah Katarina Fehling: Philipps University
Beatrice K. Koivogui: Ministère de la Santé et de l’hygiène publique
Si’Ana A. Coggins: Uniformed Services University
Eric D. Laing: Uniformed Services University
Christopher C. Broder: Uniformed Services University
Faly Magassouba N’: Ministère de la Santé et de l’hygiène publique
Thomas Strecker: Philipps University
Jeremy Rossman: University of Kent
Kader Konde: Centre for Training and Research on Priority Diseases including Malaria in Guinea
Miles W. Carroll: University of Oxford

Nature Communications, 2024, vol. 15, issue 1, 1-10

Abstract: Abstract Human Ebola virus (EBOV) outbreaks caused by persistent EBOV infection raises questions on the role of zoonotic spillover in filovirus epidemiology. To characterise filovirus zoonotic exposure, we collected cross-sectional serum samples from bushmeat hunters (n = 498) in Macenta Prefecture Guinea, adjacent to the index site of the 2013 EBOV-Makona spillover event. We identified distinct immune signatures (20/498, 4.0%) to multiple EBOV antigens (GP, NP, VP40) using stepwise ELISA and Western blot analysis and, live EBOV neutralisation (5/20; 25%). Using comparative serological data from PCR-confirmed survivors of the 2013-2016 EBOV outbreak, we demonstrated that most signatures (15/20) were not plausibly explained by prior EBOV-Makona exposure. Subsequent data-driven modelling of EBOV immunological outcomes to remote-sensing environmental data also revealed consistent associations with intact closed canopy forest. Together our findings suggest exposure to other closely related filoviruses prior to the 2013-2016 West Africa epidemic and highlight future surveillance priorities.

Date: 2024
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DOI: 10.1038/s41467-024-48587-5

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