| Literature DB >> 29154144 |
Amie J Eisfeld1, Peter J Halfmann1, Jason P Wendler2, Jennifer E Kyle2, Kristin E Burnum-Johnson2, Zuleyma Peralta3, Tadashi Maemura4, Kevin B Walters1, Tokiko Watanabe4, Satoshi Fukuyama4, Makoto Yamashita4, Jon M Jacobs2, Young-Mo Kim2, Cameron P Casey2, Kelly G Stratton5, Bobbie-Jo M Webb-Robertson5, Marina A Gritsenko2, Matthew E Monroe2, Karl K Weitz2, Anil K Shukla2, Mingyuan Tian6, Gabriele Neumann1, Jennifer L Reed6, Harm van Bakel7, Thomas O Metz8, Richard D Smith9, Katrina M Waters10, Alhaji N'jai11, Foday Sahr12, Yoshihiro Kawaoka13.
Abstract
The pathogenesis of human Ebola virus disease (EVD) is complex. EVD is characterized by high levels of virus replication and dissemination, dysregulated immune responses, extensive virus- and host-mediated tissue damage, and disordered coagulation. To clarify how host responses contribute to EVD pathophysiology, we performed multi-platform 'omics analysis of peripheral blood mononuclear cells and plasma from EVD patients. Our results indicate that EVD molecular signatures overlap with those of sepsis, imply that pancreatic enzymes contribute to tissue damage in fatal EVD, and suggest that Ebola virus infection may induce aberrant neutrophils whose activity could explain hallmarks of fatal EVD. Moreover, integrated biomarker prediction identified putative biomarkers from different data platforms that differentiated survivors and fatalities early after infection. This work reveals insight into EVD pathogenesis, suggests an effective approach for biomarker identification, and provides an important community resource for further analysis of human EVD severity.Entities:
Keywords: Ebola virus; biomarker; human; inflammation; neutrophils; omics; pancreatitis; pathogenesis; sepsis; systems biology
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Year: 2017 PMID： 29154144 PMCID： PMC5730472 DOI： 10.1016/j.chom.2017.10.011
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023