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Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: Differential transcriptional responses to Ebola and Marburg virus infection in bat and human cells
Author(s): Holzer, Martin
Krahling, Verena
Amman, Fabian
Barth, Emanuel
Bernhart, Stephan H
Collatz, Maximilian
Doose, Gero
Eggenhofer, Florian
Ewald, Jan
Fallmann, Jorg
Feldhahn, Lasse M
Fricke, Markus
Gebauer, Juliane
Wehner, Stefanie
Carmelo, Victor A O
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Keywords: Bioinformatics
Gene expression analysis
High-throughput screening
Viral infection
Issue Date: 7-Oct-2016
Citation: Holzer M, Krahling V, Amman F, Barth E, Bernhart SH, Collatz M, Doose G, Eggenhofer F, Ewald J, Fallmann J, Feldhahn LM, Fricke M, Gebauer J, Wehner S & Carmelo VAO (2016) Differential transcriptional responses to Ebola and Marburg virus infection in bat and human cells, Scientific Reports, 6, Art. No.: 24589.
Abstract: The unprecedented outbreak of Ebola in West Africa resulted in over 28,000 cases and 11,000 deaths, underlining the need for a better understanding of the biology of this highly pathogenic virus to develop specific counter strategies. Two filoviruses, the Ebola and Marburg viruses, result in a severe and often fatal infection in humans. However, bats are natural hosts and survive filovirus infections without obvious symptoms. The molecular basis of this striking difference in the response to filovirus infections is not well understood. We report a systematic overview of differentially expressed genes, activity motifs and pathways in human and bat cells infected with the Ebola and Marburg viruses, and we demonstrate that the replication of filoviruses is more rapid in human cells than in bat cells. We also found that the most strongly regulated genes upon filovirus infection are chemokine ligands and transcription factors. We observed a strong induction of the JAK/STAT pathway, of several genes encoding inhibitors of MAP kinases (DUSP genes) and of PPP1R15A, which is involved in ER stress-induced cell death. We used comparative transcriptomics to provide a data resource that can be used to identify cellular responses that might allow bats to survive filovirus infections.
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Notes: Additional co-authors: Andreas J. Gruber, Franziska Hufsky, Henrike Indrischek, Sabina Kanton, Jörg Linde, Nelly Mostajo, Roman Ochsenreiter, Konstantin Riege, Lorena Rivarola-Duarte, Abdullah H. Sahyoun, Sita J. Saunders, Stefan E. Seemann, Andrea Tanzer, Bertram Vogel, Michael T. Wolfinger, Rolf Backofen, Jan Gorodkin, Ivo Grosse, Ivo Hofacker, Steve Hoffmann, Christoph Kaleta, Peter F. Stadler, Stephan Becker, and Manja Marza

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