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    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
    UMass Chan Affiliations
    Department of Medicine
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2016-11-03
    Keywords
    UMCCTS funding
    Cell Biology
    Immunology of Infectious Disease
    Translational Medical Research
    Virology
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5115602/
    Abstract
    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.2016.10.014
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/50283
    PubMed ID
    27814506
    Notes

    Full list of authors omitted for brevity. For full list see article.

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    10.1016/j.cell.2016.10.014
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