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

Leon Louis Seifert, Clara Si, Debjani Saha, Mohammad Sadic, Maren De Vries, Sarah Ballentine, Aaron Briley, Guojun Wang, Ana M. Valero-Jimenez, Adil Mohamed, Uwe Schaefer, Hong M. Moulton, Adolfo García-Sastre, Shashank Tripathi, Brad R. Rosenberg, Meike Dittmann

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29 Scopus citations

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.

Original languageEnglish
Article numbere1007634
JournalPLoS Pathogens
Volume15
Issue number11
DOIs
StatePublished - 2019

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