Transmission models indicate Ebola virus persistence in non-human primate populations is unlikely.

David T. S. Hayman,Reju Sam John,Pejman Rohani

doi:10.1098/rsif.2021.0638

David T. S. Hayman, Reju Sam John + Show 1 more

Open Access

https://doi.org/10.1098/rsif.2021.0638

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Abstract

Infectious diseases that kill their hosts may persist locally only if transmission is appropriately balanced by susceptible recruitment. Great apes die of Ebola virus disease (EVD) and have transmitted ebolaviruses to people. However, understanding the role that apes and other non-human primates play in maintaining ebolaviruses in Nature is hampered by a lack of data. Recent serological findings suggest that few non-human primates have antibodies to EVD-causing viruses throughout tropical Africa, suggesting low transmission rates and/or high EVD mortality (Ayouba A et al. 2019 J. Infect. Dis. 220, 1599–1608 (doi:10.1093/infdis/jiz006); Mombo IM et al. 2020 Viruses 12, 1347 (doi:10.3390/v12121347)). Here, stochastic transmission models of EVD in non-human primates assuming high case-fatality probabilities and experimentally observed or field-observed parameters did not allow viral persistence, suggesting that non-human primate populations are highly unlikely to sustain EVD-causing infection for prolonged periods. Repeated introductions led to declining population sizes, similar to field observations of apes, but not viral persistence.

Highlights

IntroductionAlmost half of the Ebola virus disease (EVD)-infected people die and mortality from EVD is thought to have caused massive declines in Central African apes [1,2]
Ebola virus disease (EVD) kills apes: both people and the great apes of Africa
Previous work has modelled the impact of EVD on ape populations and their recovery [59]

Summary

Introduction

Almost half of the EVD-infected people die and mortality from EVD is thought to have caused massive declines in Central African apes [1,2]. Infections that cause high mortality rates are thought to reduce their likelihood of onward transmission because death removes infected hosts [3,4]. This higher mortality, or pathogenicity, is one of the reasons so-called ‘spillover’ events of infectious agents from one species or group of species that form a reservoir to new hosts fail to persist in those new host populations. Global case-fatality studies for infectious diseases of domestic mammals suggest that the evolutionary distance from an infected host to other hosts is a strong predictor of diseaseinduced mortality [5]. Infections are expected to optimize the level of virulence (which may include pathogenic effects) to optimize their fitness, often characterized through the basic reproductive number (R0) [4,8]

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