Author: Selinger, Christian; Tisoncik-Go, Jennifer; Menachery, Vineet D; Agnihothram, Sudhakar; Law, G Lynn; Chang, Jean; Kelly, Sara M; Sova, Pavel; Baric, Ralph S; Katze, Michael G
Title: Cytokine systems approach demonstrates differences in innate and pro-inflammatory host responses between genetically distinct MERS-CoV isolates Document date: 2014_12_22
ID: 0y3m47lh_11
Snippet: Topological analysis of gene expression restricted to IFN and pro-inflammatory cytokine genes sets revealed IFN induction (score: 0.74) as a major contributor to kinetic differences between MERS-CoV SA 1 and MERS-CoV IFN-γ responses, as well as enrichment of genes associated with adaptive immune responses such as OX40 signaling and cytotoxic T lymphocyte-mediated apoptosis pathways. IFN-α response genes were significantly enriched for cellular .....
Document: Topological analysis of gene expression restricted to IFN and pro-inflammatory cytokine genes sets revealed IFN induction (score: 0.74) as a major contributor to kinetic differences between MERS-CoV SA 1 and MERS-CoV IFN-γ responses, as well as enrichment of genes associated with adaptive immune responses such as OX40 signaling and cytotoxic T lymphocyte-mediated apoptosis pathways. IFN-α response genes were significantly enriched for cellular pathways involved in the antiviral response, such as interferon regulatory factor (IRF) activation by pathogen recognition receptors (PRRs). Pro-inflammatory mediators, IL-1α and TNF, which stimulate genes related to IL-17 signaling, were identified following MERS infection. For example, pro-inflammatory cytokine genes, CXCL1, CCL2, and CCL20, regulated by IL-17A [23] and play a prominent role in airway inflammation and disease, and NF-κB genes, NFKBIA, NFKB2 and NFKBIE, were all found to be DE in response to TNF and MERS-CoV infection.
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