Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic
AuthorsDiehl, William E.
Kyawe, Pyae Phyo
McCauley, Sean M.
McDonel, Patrick E.
Document TypeJournal Article
Immunology of Infectious Disease
Translational Medical Research
MetadataShow full item record
AbstractThe 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.
Cell. 2016 Nov 3;167(4):1088-1098.e6. doi: 10.1016/j.cell.2016.10.014. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/50283
Full list of authors omitted for brevity. For full list see article.