Abstract
The Ebola virus (EBOV) variant Makona (which emerged in 2013) was the causative agent of the largest outbreak of Ebola Virus Disease recorded. Differences in virus-host interactions between viral variants have potential consequences for transmission, disease severity and mortality. A detailed profile of the cellular changes induced by the Makona variant compared with other Ebola virus variants was lacking. In this study, A549 cells, a human cell line with a robust innate response, were infected with the Makona variant or with the Ecran variant originating from the 1976 outbreak in Central Africa. The abundance of viral and cellular mRNA transcripts was profiled using RNASeq and differential gene expression analysis performed. Differences in effects of each virus on the expression of interferon-stimulated genes were also investigated in A549 NPro cells where the type 1 interferon response had been attenuated. Cellular transcriptomic changes were compared with those induced by human respiratory syncytial virus (HRSV), a virus with a similar genome organisation and replication strategy to EBOV. Pathway and gene ontology analysis revealed differential expression of functionally important genes; including genes involved in the inflammatory response, cell proliferation, leukocyte extravasation and cholesterol biosynthesis. Whilst there was overlap with HRSV, there was unique commonality to the EBOV variants.
Original language | English |
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Article number | 43144 |
Journal | Scientific Reports |
Volume | 7 |
DOIs | |
Publication status | Published - 27 Feb 2017 |
Bibliographical note
Funding Information:High containment work was supported by the High Containment Microbiology group, National Infection Service, Public Health England, Porton Down, UK. The work was supported by funding from the Centre of Defence Enterprise (UK) to D.A.M., J.S. and J.A.H. This work was also funded by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Emerging and Zoonotic Infections at the University of Liverpool in partnership with Public Health England (PHE) and the Liverpool School of Tropical Medicine awarded to J.A.H., R.H. and M.W.C. The views expressed are those of the authors and not necessarily those of the National Health Service, the NIHR, The University of Liverpool, The Department of Health or P.H.E. We would like to thank Prof. Steve Goodbourn at St. George's, University of London, for the use of the A549 NPro cell line.
Publisher Copyright:
© 2017 The Author(s).