Assessing the contribution of interferon antagonism to the virulence of West African Ebola viruses
Eric C. Dunham,
Logan Banadyga,
Allison Groseth,
Abhilash I. Chiramel,
Sonja M. Best,
Hideki Ebihara,
Heinz Feldmann and
Thomas Hoenen ()
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Eric C. Dunham: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Logan Banadyga: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Allison Groseth: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Abhilash I. Chiramel: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Sonja M. Best: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Hideki Ebihara: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Heinz Feldmann: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Thomas Hoenen: Laboratory of Virology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Nature Communications, 2015, vol. 6, issue 1, 1-6
Abstract:
Abstract The current Ebola virus (EBOV) outbreak in West Africa is unprecedented in terms of both its size and duration, and there has been speculation and concern regarding the potential for EBOV to increase in virulence as a result of its prolonged circulation in humans. Here we investigate the relative potency of the interferon (IFN) inhibitors encoded by EBOVs from West Africa, since an important EBOV virulence factor is inhibition of the antiviral IFN response. Based on this work we show that, in terms of IFN antagonism, the West African viruses display no discernible differences from the prototype Mayinga isolate, which corroborates epidemiological data suggesting these viruses show no increased virulence compared with those from previous outbreaks. This finding has important implications for public health decisions, since it does not provide experimental support for theoretical claims that EBOV might gain increased virulence due to the extensive human-to-human transmission in the on-going outbreak.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9000
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DOI: 10.1038/ncomms9000
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