Differential transcriptional responses to Ebola and Marburg virus infection in bat and human cells
Citations Over TimeTop 10% of 2016 papers
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.
Related Papers
- → Post-exposure immunotherapy for two ebolaviruses and Marburg virus in nonhuman primates(2019)60 cited
- → Approaches to demonstrating the effectiveness of filovirus vaccines: Lessons from Ebola and COVID-19(2023)9 cited
- → Sudan Ebolavirus VP35-NP Crystal Structure Reveals a Potential Target for Pan-Filovirus Treatment(2019)14 cited
- → Design and evaluation of bi- and trispecific antibodies targeting multiple filovirus glycoproteins(2018)13 cited
- Comprehensive Profiling of Immune Responses in MARV Survivors Demonstrates Robust Th1-Skewing with Short-Lived Neutralizing Antibody Responses(2017)