Journal
CELL
Volume 161, Issue 7, Pages 1516-1526Publisher
CELL PRESS
DOI: 10.1016/j.cell.2015.06.007
Keywords
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Funding
- European Union grant FP7 [278433-PREDEMICS]
- European Research Council [260864]
- Natural Environment Research Council [D76739X]
- NIH [U54 GM111274, GM080177, 1U01HG007480-01]
- National Science Foundation Graduate Research Fellowship [DGE 1144152]
- National Health and Medical Research Council, Australia
- Defense Threat Reduction Agency (USAMRIID)
- NIH/NIAID (Broad Institute) [U19AI110818]
- Bill and Melinda Gates Foundation (Broad Institute) [OPP1123407]
- US National Institute of Allergy and Infectious Diseases (NIAID) [HHSN272200700016I]
- National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services [HHSN272201400028C]
- NIAID (Harvard/Tulane) [HHSN272200900049C]
- Zalgen Labs
- Bill and Melinda Gates Foundation [OPP1123407] Funding Source: Bill and Melinda Gates Foundation
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The 2013-2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission and offered important information for outbreak response. Here, we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission.
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