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Viruses are recognized by receptors of the innate immune system, which leads, among other things, to the induction of antiviral type I interferons (IFNs) (1). After their release, type I IFNs recruit professional immune cells and induce a broad transcriptional program of hundreds of interferon-stimulated genes (ISGs) in an autocrine and paracrine manner.
Interferon-stimulated genes (ISGs) not only encode antiviral restriction factors but also nucleic acid receptors and signaling components themselves, enabling the amplification and diversification of immune signaling within the originally stimulated cell and those responding in a paracrine manner (2)
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