Park Daniel J, Dudas Gytis, Wohl Shirlee, Goba Augustine, Whitmer Shannon L M, Andersen Kristian G, Sealfon Rachel S, Ladner Jason T, Kugelman Jeffrey R, Matranga Christian B, Winnicki Sarah M, Qu James, Gire Stephen K, Gladden-Young Adrianne, Jalloh Simbirie, Nosamiefan Dolo, Yozwiak Nathan L, Moses Lina M, Jiang Pan-Pan, Lin Aaron E, Schaffner Stephen F, Bird Brian, Towner Jonathan, Mamoh Mambu, Gbakie Michael, Kanneh Lansana, Kargbo David, Massally James L B, Kamara Fatima K, Konuwa Edwin, Sellu Josephine, Jalloh Abdul A, Mustapha Ibrahim, Foday Momoh, Yillah Mohamed, Erickson Bobbie R, Sealy Tara, Blau Dianna, Paddock Christopher, Brault Aaron, Amman Brian, Basile Jane, Bearden Scott, Belser Jessica, Bergeron Eric, Campbell Shelley, Chakrabarti Ayan, Dodd Kimberly, Flint Mike, Gibbons Aridth, Goodman Christin, Klena John, McMullan Laura, Morgan Laura, Russell Brandy, Salzer Johanna, Sanchez Angela, Wang David, Jungreis Irwin, Tomkins-Tinch Christopher, Kislyuk Andrey, Lin Michael F, Chapman Sinead, MacInnis Bronwyn, Matthews Ashley, Bochicchio James, Hensley Lisa E, Kuhn Jens H, Nusbaum Chad, Schieffelin John S, Birren Bruce W, Forget Marc, Nichol Stuart T, Palacios Gustavo F, Ndiaye Daouda, Happi Christian, Gevao Sahr M, Vandi Mohamed A, Kargbo Brima, Holmes Edward C, Bedford Trevor, Gnirke Andreas, Ströher Ute, Rambaut Andrew, Garry Robert F, Sabeti Pardis C
Broad Institute of Harvard and MIT, 75 Ames Street, Cambridge, MA 02142, USA.
Institute of Evolutionary Biology, Ashworth Laboratories, University of Edinburgh, Edinburgh EH9 3FL, UK.
Cell. 2015 Jun 18;161(7):1516-26. doi: 10.1016/j.cell.2015.06.007.
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.
2013 - 2015年埃博拉病毒病（EVD）疫情由埃博拉病毒（EBOV）的马科纳变种引起。在疫情早期，基因组测序为病毒进化和传播提供了见解，并为疫情应对提供了重要信息。在此，我们分析了在塞拉利昂7个月内采样的232名患者的序列，以及疫情早期公布的86个基因组。我们证实了塞拉利昂境内持续的人际传播，并且没有发现EBOV在初次引入后跨境输入或输出的证据。通过深度重复测序，我们观察到了宿主间传播以及宿主内遗传变异的反复出现。我们追踪了纯化选择在抑制非同义突变积累方面随时间增加的影响。最后，我们注意到EBOV糖蛋白粘蛋白样结构域的变化值得进一步研究。这些发现阐明了EBOV在该地区的传播情况，并描述了在长时间人际传播期间的病毒进化。
