Serological evidence of zoonotic filovirus exposure among bushmeat hunters in Guinea

Abstract

Recent human Ebola virus (EBOV) outbreaks caused by persistent EBOV infection raised questions on the role of zoonotic spillover in filovirus epidemiology. To characterise potential historical 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 a 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 past exposure to other closely related filoviruses prior to the 2013–2016 west African epidemic and highlight future surveillance priorities.

rVSV-ZEBOV vaccination in people with pre-existing immunity to Ebolavirus: an open-label safety and immunogenicity study in Guinean communities affected by Ebola virus disease (l’essai Proches)

“…7,29 The nding that 16.3% of proches had detectable IgG to EBOV-GP is consistent with previous community/contact studies in central Africa, [14][15][16][17][18] and warrants further investigation into the prevalence of asymptomatic cases and the mechanisms behind asymptomatic or abortive EBOV infections. 30 Researchers found ~15% of study participants in Guinea, Sierra Leone, Liberia in 2018 had prior EBOV-GP immunity before vaccination compared to only 5% in neighbouring Mali. 31 Proposals for this seemingly higher level of seroprevalence include the geographical and ecological differences between these two regions and prior exposure to related and potentially non-pathogenic loviruses, such exposures may account for some of the elevated baseline responses seen in this study.…”