Assessing the contribution of interferon antagonism to the virulence of West African Ebola viruses

• Published in: Nature communications Vol. 6; no. 1; p. 8000
• Main Authors: Dunham, Eric C., Banadyga, Logan, Groseth, Allison, Chiramel, Abhilash I., Best, Sonja M., Ebihara, Hideki, Feldmann, Heinz, Hoenen, Thomas
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 05.08.2015; Nature Publishing Group
• Subjects: 38/109; 38/70; 631/250/127/1212; 631/326/596/2042; Africa, Western; Cloning, Molecular; Coding; Decision theory; Disease transmission; Ebola virus; Ebolavirus; Ebolavirus - genetics; Ebolavirus - pathogenicity; Epidemiology; HEK293 Cells; Humanities and Social Sciences; Humans; Interferon; Interferon-beta - antagonists & inhibitors; multidisciplinary; Outbreaks; Public health; Science; Science (multidisciplinary); Viral diseases; Viral Proteins - chemistry; Viral Proteins - genetics; Viral Regulatory and Accessory Proteins - chemistry; Viral Regulatory and Accessory Proteins - genetics; Virulence; Virulence factors; Viruses; Africa, Western; West Africa
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/ncomms9000

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. Concerns have been raised regarding potential increase in the virulence of the Ebola virus during the current West African outbreak. Here the authors show that the ability to inhibit interferon response, one of the aspects of Ebola virus virulence, does not differ between the prototype Mayinga and isolates from the current outbreak.