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

被引：16

作者：

Dunham, Eric C. ^{[1
]}

Banadyga, Logan ^{[1
]}

Groseth, Allison ^{[1
]}

Chiramel, Abhilash I. ^{[1
]}

Best, Sonja M. ^{[1
]}

Ebihara, Hideki ^{[1
]}

Feldmann, Heinz ^{[1
]}

Hoenen, Thomas ^{[1
]}

机构：

[1] NIAID, Virol Lab, Div Intramural Res, NIH, Hamilton, MT 59840 USA

来源：

NATURE COMMUNICATIONS | 2015年 / 6卷

关键词：

HEMORRHAGIC-FEVER VIRUSES; DOUBLE-STRANDED-RNA; VP35; PROTEIN; KARYOPHERIN ALPHA-1; INHIBITORY DOMAIN; NUCLEAR IMPORT; MARBURG-VIRUS; VP24; REPLICATION; TRANSCRIPTION;

D O I：

10.1038/ncomms9000

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：6

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