Changes in critical sites of virus-encoded protein or cis-acting element generally determine pathogenicity differentiation among different isolates of the same plant virus. Cucumber mosaic virus (CMV) isolates, which exhibit the most extensively known host range, demonstrate notable pathogenicity differentiation. This study focuses on the severe isolate CMVFny and mild isolate CMVTA-pe, both affecting several species within the Solanaceae family, to identify the key factors regulating pathogenicity differentiation. Through a pseudo-recombination assay, the principal RNA segments regulating the pathogenicity of two CMV isolates were localized to RNA1 and RNA2, with a particular emphasis on RNA2. By generating chimeric mutants on RNA1 or RNA2 of the two isolates, the pathogenicity differentiation was suggested to be mainly associated with protein 1a of RNA1 as well as the synergistic interactions involving protein 2a as well as the 5'-untranslated region (UTR) and the 3'-UTR of RNA2. Moreover, the influence of protein 1a of RNA1 and protein 2a, 5'-UTR, and 3'-UTR of RNA2 on pathogenicity differentiation exhibited a coevolutionary pattern. This coevolutionary pattern of proteins 1a and 2a, along with the UTRs of RNA2, was also corroborated in three additional CMV isolates: CMVZMBJ, CMVWF-Ch, and CMVJN-Cu. In addition, multiple phylogenetic tree analyses revealed a synchronous evolutionary pattern among proteins 1a and 2a and the 5'-UTR and 3'-UTR of RNA2. This study provided new insights into the pathogenicity differentiation of RNA viruses.
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