RNA viruses, as obligate intracellular parasites, rely on the host cell machinery for replication, making them powerful models to study the rewiring of cellular gene expression networks. The compact viral genomes contain many intricately folded RNA structure elements that enable the manipulation of host pathways. Viral RNA structures rival proteins in both functional versatility and necessity for the viral life cycle. Yet unlike proteins, the structure-function relationships of viral RNA structures remain strikingly underexplored. Our research program addresses this critical knowledge gap by integrating structural biology, RNA biochemistry, high-throughput functional assays and cellular virology. A major focus of the lab is on viral RNA structures known as exoribonuclease-resistant RNAs (xrRNAs). XrRNAs efficiently halt degradation by cellular exoribonucleases at precise sites in the viral genome, leading to the accumulation of partially degraded viral genomes that function as subgenomic RNAs (sgRNAs) with crucial roles in viral replication and immune evasion. Initially discovered in West Nile virus and related flaviviruses over a decade ago, we recently discovered hundreds of additional nuclease-resistant xrRNA structures in the genomes of plant-infecting RNA viruses. This widespread prevalence suggests that nuclease-resistance is a common viral strategy for sgRNA maturation. We present structural and biophysical data demonstrating that xrRNAs from plant-infecting viruses xrRNA share a core structural motif - a protective ring encircling the RNA's 5′ end – with human-pathogenic flaviviruses, despite lacking sequence similarity. This finding demonstrates that distantly related RNA viruses have converged on a common structural strategy to inhibit cellular nucleases, uncovering universal principles of xrRNA folding.