Key result
Enterovirus coxsackiepol ciRNA function requires a conserved loop E motif and long-range base-pairing.
Why the study?
The evolutionary conservation and structural requirements of the poliovirus serotype 1 competitive inhibitor RNA (ciRNA) that inhibits host RNase L were previously unexplored.
The dual constraints of encoding a protein and forming a specific functional structure limit the sequence diversity and phylogenetic distribution of enterovirus ciRNAs.
May guide enterovirus antiviral design; leaves open in vivo validation and broader picornavirus applicability.
RNA molecules form specific 3D structures that facilitate a variety of functions through interactions with other macromolecules. Many RNA viral genomes maintain these structures to interact with and evade host immunity machinery. One such element, the competitive inhibitor RNA (ciRNA), discovered in the protein coding region of the poliovirus serotype 1 (PV1) genome, inhibits a host antiviral protein, ribonuclease L (RNase L). Although some functionally essential structural motifs of the PV1 ciRNA have been studied, the extent of its evolutionary conservation and other structural requirements remained unexplored. Here we combined bioinformatic and biochemical techniques to further define the requirements of a functional ciRNA and assess its phylogenetic distribution. We systematically mutated ciRNA structural features, verifying that ciRNA inhibitory activity requires a conserved loop E motif and a long-range base-pairing interaction, but its peripheral stems are dispensable and in fact a circularly permuted version maintains function. A structure-based homology search identified potential ciRNAs across the Picornaviridae family, but only a subset of those tested were functional-all are in Enterovirus coxsackiepol. When structural features needed for function were transposed from PV1 ciRNA to an RNA unable to inhibit RNase L, the chimeric RNAs did not gain wild-type function, and chemical probing data revealed that these nonfunctional RNAs are unable to form the correct secondary structure. Overall, the dual constraints of encoding a protein and forming a specific functional structure appear to not only limit the sequence diversity, but also the phylogenetic distribution, of ciRNAs.
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Zangari et al. (2026) studied Enterovirus infection. ciRNA structural mutations vs. Wild-type ciRNA was evaluated on ciRNA inhibitory activity against RNase L. Competitive inhibitor RNA (ciRNA) function requires a conserved loop E motif and long-range base-pairing, with its phylogenetic distribution limited to Enterovirus coxsackiepol.
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