Abstract

Following its immergence in December 2013, the recent Zaire Ebola virus (EBOV) outbreak in West Africa has spread and persisted for more than two years, making it the largest EBOV epidemic in both scale and geographical region to date. In this study, a total of 726 glycoprotein (GP) gene sequences of the EBOV full-length genome obtained from West Africa from the 2014 outbreak, combined with 30 from earlier outbreaks between 1976 and 2008 were used to investigate the genetic divergence, evolutionary history, population dynamics, and selection pressure of EBOV among distinct epidemic waves. Results from our dataset showed that no non-synonymous substitutions occurred on the GP gene coding sequences of EBOV that were likely to have affected protein structure or function in any way. Furthermore, the significantly different dN/dS ratios observed between the 2014 West African outbreak and earlier outbreaks were more likely due to the confounding presence of segregating polymorphisms. Our results highlight no robust evidence that the 2014 EBOV outbreak is fast-evolving and adapting to humans. Therefore, the unprecedented nature of the 2014 EBOV outbreak might be more likely related to non-virological elements, such as environmental and sociological factors.

Highlights

  • The Zaire Ebola virus (EBOV), a member of the Filoviridae family, is an enveloped, non-segmented, negative strand RNA virus approximately 19 kb in length, which has caused considerable morbidity and mortality in West African human populations[1]

  • Phylogenetic analyses of both RAxML and GARLI trees confirmed the phylogenetic position shown in recent study[4] and divided the EBOV epidemics into six lineages based on the temporality of each epidemic wave and phylogenetic clustering (Fig. S1)

  • We further investigated the population dynamics of the 1976–2015 EBOV by estimating a coalescent-based Bayesian skygrid plot for the dataset[28], which depicted the changes in effective population size over time

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Summary

Introduction

The Zaire Ebola virus (EBOV), a member of the Filoviridae family, is an enveloped, non-segmented, negative strand RNA virus approximately 19 kb in length, which has caused considerable morbidity and mortality in West African human populations[1]. EBOV is the causative agent of Ebola virus disease (EVD), which was first isolated and identified in 1976 during a hemorrhagic fever epidemic in the Democratic Republic of Congo (DRC) ( known as Zaire, with the outbreak epicenter located in Yambuku), with cases reported in several districts of Guinea, suggesting a hidden, at that point, history of pandemic spread in Africa. Understanding the natural selection that has shaped genetic variation is a critical aspect for the evaluation of how certain pathogens adapt to host populations. Identification of genes or genomic regions that have been targeted by natural selection, pinpointing the genotypic variation that causes a certain pathogen to adapt to a host population, is essential for the development of vaccines and therapeutics.

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