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The ETS transcription factor ELF1 regulates a broadly antiviral program distinct from the type I interferon response

Authors: 
Seifert LL, Si C, Saha D, Sadic M, de Vries M, Ballentine S, Briley A, Wang G, Valero-Jimenez AM, Mohamed A, Schaefer U, Moulton HM, GarcĂ­a-Sastre A, Tripathi S, Rosenberg BR, Dittmann M
Citation: 
PLoS Pathog. 2019 Nov 4;15(11):e1007634. doi: 10.1371/journal.ppat.1007634. [Epub ahead of print]
Abstract: 
Induction of vast transcriptional programs is a central event of innate host responses to viral infections. Here we report a transcriptional program with potent antiviral activity, driven by E74-like ETS transcription factor 1 (ELF1). Using microscopy to quantify viral infection over time, we found that ELF1 inhibits eight diverse RNA and DNA viruses after multi-cycle replication. Elf1 deficiency results in enhanced susceptibility to influenza A virus infections in mice. ELF1 does not feed-forward to induce interferons, and ELF1's antiviral effect is not abolished by the absence of STAT1 or by inhibition of JAK phosphorylation. Accordingly, comparative expression analyses by RNA-seq revealed that the ELF1 transcriptional program is distinct from interferon signatures. Thus, ELF1 provides an additional layer of the innate host response, independent from the action of type I interferons.
Organism or Cell Type: 
mice
Delivery Method: 
intranasal peptide-linked