• Daniel J Park, Gytis Dudas, Shirlee Wohl, Augustine Goba, Shannon L M Whitmer, Kristian G Andersen, Rachel S Sealfon, Jason T Ladner, Jeffrey R Kugelman, Christian B Matranga, Sarah M Winnicki, James Qu, Stephen K Gire, Adrianne Gladden-Young, Simbirie Jalloh, Dolo Nosamiefan, Nathan L Yozwiak, Lina M Moses, Pan-Pan Jiang, Aaron E Lin, Stephen F Schaffner, Brian Bird, Jonathan Towner, Mambu Mamoh, Michael Gbakie, Lansana Kanneh, David Kargbo, James L B Massally, Fatima K Kamara, Edwin Konuwa, Josephine Sellu, Abdul A Jalloh, Ibrahim Mustapha, Momoh Foday, Mohamed Yillah, Bobbie R Erickson, Tara Sealy, Dianna Blau, Christopher Paddock, Aaron Brault, Brian Amman, Jane Basile, Scott Bearden, Jessica Belser, Eric Bergeron, Shelley Campbell, Ayan Chakrabarti, Kimberly Dodd, Mike Flint, Aridth Gibbons, Christin Goodman, John Klena, Laura McMullan, Laura Morgan, Brandy Russell, Johanna Salzer, Angela Sanchez, David Wang, Irwin Jungreis, Christopher Tomkins-Tinch, Andrey Kislyuk, Michael F Lin, Sinead Chapman, Bronwyn MacInnis, Ashley Matthews, James Bochicchio, Lisa E Hensley, Jens H Kuhn, Chad Nusbaum, John S Schieffelin, Bruce W Birren, Marc Forget, Stuart T Nichol, Gustavo F Palacios, Daouda Ndiaye, Christian Happi, Sahr M Gevao, Mohamed A Vandi, Brima Kargbo, Edward C Holmes, Trevor Bedford, Andreas Gnirke, Ute Ströher, Andrew Rambaut, Robert F Garry, and Pardis C Sabeti.
• Broad Institute of Harvard and MIT, 75 Ames Street, Cambridge, MA 02142, USA. Electronic address: dpark@broadinstitute.org.
• Cell. 2015 Jun 18;161(7):1516-26.

AbstractThe 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.Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

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