Human Adaptation of Ebola Virus during the West African Outbreak

The 2013-2016 outbreak of Ebola virus (EBOV) in West Africa was the largest recorded. It began following the cross-species transmission of EBOV from an animal reservoir, most likely bats, into humans, with phylogenetic analysis revealing the co-circulation of several viral lineages. We hypothesized...

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Veröffentlicht in:Cell Jg. 167; H. 4; S. 1079
Hauptverfasser: Urbanowicz, Richard A, McClure, C Patrick, Sakuntabhai, Anavaj, Sall, Amadou A, Kobinger, Gary, Müller, Marcel A, Holmes, Edward C, Rey, Félix A, Simon-Loriere, Etienne, Ball, Jonathan K
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 03.11.2016
Schlagworte:
Africa, Western - epidemiology
Animals
Biological Evolution
Chiroptera - virology
Disease Outbreaks
Ebolavirus - classification
Ebolavirus - genetics
Ebolavirus - pathogenicity
Ebolavirus - physiology
Hemorrhagic Fever, Ebola - epidemiology
Hemorrhagic Fever, Ebola - transmission
Hemorrhagic Fever, Ebola - virology
Host Specificity
Humans
Mutation
Phylogeny
Viral Envelope Proteins - genetics
Viral Envelope Proteins - metabolism
Zoonoses
Ebola virus
pseudovirus
bat
epistasis
Makona
tropism
adaptation
evolution
human
ISSN:1097-4172, 1097-4172
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Zusammenfassung:The 2013-2016 outbreak of Ebola virus (EBOV) in West Africa was the largest recorded. It began following the cross-species transmission of EBOV from an animal reservoir, most likely bats, into humans, with phylogenetic analysis revealing the co-circulation of several viral lineages. We hypothesized that this prolonged human circulation led to genomic changes that increased viral transmissibility in humans. We generated a synthetic glycoprotein (GP) construct based on the earliest reported isolate and introduced amino acid substitutions that defined viral lineages. Mutant GPs were used to generate a panel of pseudoviruses, which were used to infect different human and bat cell lines. These data revealed that specific amino acid substitutions in the EBOV GP have increased tropism for human cells, while reducing tropism for bat cells. Such increased infectivity may have enhanced the ability of EBOV to transmit among humans and contributed to the wide geographic distribution of some viral lineages.
Bibliographie:ObjectType-Article-1
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ISSN:1097-4172
1097-4172
DOI:10.1016/j.cell.2016.10.013