Abstract

We generated genome sequences from 218 cases of Ebola virus disease (EVD) in Sierra Leone (SLE) during 2014–2015 to complement available datasets, particularly by including cases from a period of low sequence coverage during peak transmission of Ebola virus (EBOV) in the highly-affected Western Area division of SLE. The combined dataset was utilized to produce phylogenetic and phylodynamic inferences, to study sink–source dynamics and virus dispersal from highly-populated transmission hotspots. We identified four districts in SLE where EBOV was introduced and transmission occurred without onward exportation to other districts. We also identified six districts that substantially contributed to the dispersal of the virus and prolonged the EVD outbreak: five of these served as major hubs, with lots of movement in and out, and one acted primarily as a source, exporting the virus to other areas of the country. Positive correlations between case numbers, inter-district transition events, and district population sizes reaffirm that population size was a driver of EBOV transmission dynamics in SLE. The data presented here confirm the role of urban hubs in virus dispersal and of a delayed laboratory response in the expansion and perpetuation of the EVD outbreak in SLE.

Highlights

  • Between 2013 and 2016, the West African countries of Guinea, Liberia, Sierra Leone, Nigeria, and Mali reported the largest outbreak of Ebola virus disease (EVD) in recorded history, with 28,646 documented cases, of which 11,323 were fatal [1,2]

  • Based on the best-fit slope, there was an increase of one case per 333 people

  • EVD outbreaks before the 2013–2016 West Africa outbreak were limited to rural areas, and spread outbreaks before the 2013–2016

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Summary

Introduction

Between 2013 and 2016, the West African countries of Guinea, Liberia, Sierra Leone, Nigeria, and Mali reported the largest outbreak of Ebola virus disease (EVD) in recorded history, with 28,646 documented cases, of which 11,323 were fatal [1,2]. Molecular studies revealed that the SLE portion of the outbreak, which occurred largely in isolation with concurrent outbreaks in Liberia and Guinea, originated from the introduction of two distinct lineages (SL1 and SL2) of the Makona variant of Ebola virus (EBOV) from Guinea into eastern. The SL3 lineage responsible for the majority of cases in SLE, evolved later in the background of SL2, and was initially characterized by a single mutation at genome position 10,218 (G>A in the untranslated region of VP24).

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