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Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic.

Cell | Nov 3, 2016

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.

Pubmed ID: 27814506 RIS Download

Mesh terms: Africa, Western | Amino Acid Substitution | Animals | Callithrix | Carrier Proteins | Cheirogaleidae | Cytoplasm | Ebolavirus | Hemorrhagic Fever, Ebola | Humans | Membrane Glycoproteins | Protein Conformation, alpha-Helical | Viral Envelope Proteins | Virion | Virulence

Data used in this publication

None found

Associated grants

  • Agency: NCATS NIH HHS, Id: UL1 TR001114
  • Agency: NHGRI NIH HHS, Id: U01 HG007910
  • Agency: NCATS NIH HHS, Id: UL1 TR001453
  • Agency: NIAID NIH HHS, Id: R01 AI111809
  • Agency: NIAID NIH HHS, Id: T32 AI007244
  • Agency: NIDA NIH HHS, Id: DP1 DA034990
  • Agency: NIAID NIH HHS, Id: U19 AI110818
  • Agency: NIAID NIH HHS, Id: HHSN272201400048C

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