ILF3 contributes to the establishment of the antiviral type I interferon program

Samir F Watson, Nicolas Bellora, Sara Macias

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1, and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised.
Original languageEnglish
Article numbergkz1060
Pages (from-to)116-129
Number of pages14
JournalNucleic Acids Research
Issue number1
Early online date8 Nov 2019
Publication statusPublished - 10 Jan 2020


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