Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic
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Authors
Diehl, William E.Kim, Kyusik
Kyawe, Pyae Phyo
McCauley, Sean M.
Donnard, Elisa
Kucukural, Alper
McDonel, Patrick E.
Garber, Manuel
Luban, Jeremy
Document Type
Journal ArticlePublication Date
2016-11-03Keywords
UMCCTS fundingCell Biology
Immunology of Infectious Disease
Translational Medical Research
Virology
Metadata
Show full item recordAbstract
The magnitude of the 2013-2016 Ebola virus disease (EVD) epidemic enabled an unprecedented number of viral mutations to occur over successive human-to-human transmission events, increasing the probability that adaptation to the human host occurred during the outbreak. We investigated one nonsynonymous mutation, Ebola virus (EBOV) glycoprotein (GP) mutant A82V, for its effect on viral infectivity. This mutation, located at the NPC1-binding site on EBOV GP, occurred early in the 2013-2016 outbreak and rose to high frequency. We found that GP-A82V had heightened ability to infect primate cells, including human dendritic cells. The increased infectivity was restricted to cells that have primate-specific NPC1 sequences at the EBOV interface, suggesting that this mutation was indeed an adaptation to the human host. GP-A82V was associated with increased mortality, consistent with the hypothesis that the heightened intrinsic infectivity of GP-A82V contributed to disease severity during the EVD epidemic.Source
Cell. 2016 Nov 3;167(4):1088-1098.e6. doi: 10.1016/j.cell.2016.10.014. Link to article on publisher's site
DOI
10.1016/j.cell.2016.10.014Permanent Link to this Item
http://hdl.handle.net/20.500.14038/50283PubMed ID
27814506Notes
Full list of authors omitted for brevity. For full list see article.
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10.1016/j.cell.2016.10.014