RIG-I detects viral genomic RNA during negative-strand RNA virus infection.

By J. Rehwinkel, C. Tan, D. Goubau, O. Schulz, A. Pichlmair, K. Bier, Nicole C. Robb, F. Vreede, W. Barclay, E. Fodor and 1 more. Cell, 2010

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RIG-I uses an ATPase-powered translocation-throttling mechanism for kinetic proofreading of RNAs and oligomerization (2018, background): “many viral RNA genomes and replication intermediates (Hornung et al., 2006; Rehwinkel et al., 2010; Schlee et al., 2009).”
Preference of RIG-I for short viral RNA molecules in infected cells revealed by next-generation sequencing (2010, background): “A recent study using overexpressed RIG-I has shown that this protein associates with negative stranded viral RNA in Sendai virus-infected (SeV) cells and concluded that genomic RNA serves as a inducer of RIG-I signaling (3).”
From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “Sendai virus (SeV) can induce pyroptosis, apoptosis and necroptosis (Table 2) and RIG-I is the viral sensor to trigger interferon production in this context [138].”
Influenza A Virus Panhandle Structure Is Directly Involved in RIG-I Activation and Interferon Induction (2015, background): “stitution was performed as described elsewhere (15).”
A structure-based model of RIG-I activation. (2012, background): “Nevertheless, panhandle structures corresponding to the blunt-ended 59pppbpRNAs that act as RIG-I PAMPs in vitro occur in many ssRNA virus systems and have been implicated (Strahle et al. 2007; Schlee et al. 2009; Baum et al. 2010; Rehwinkel et al. 2010).”