The U2 snRNP moonlights as an antiviral complex. Schematic representation of the working model by which the U2 snRNP might suppress the infection of cytoplasmic viruses. It represents two potential working models on how the relocated U2 snRNP components recognize viral RNA: (1) through a direct scanning of viral RNA seeking for accessible complementary sequences to the U2 snRNA, and (2) recruitment of the U2 snRNP to the targeted regions by adaptor complexes with high specificity. For example, U2AF1, U2AF2, and SF1 play a crucial role in branching point recognition, which enables the recruitment of the U2 snRNP (Wahl et al. 2009). A similar mechanism may occur at VROs, with U2AF1–U2AF2–SF1 or an unknown complex depositing the U2 snRNP at a branching point-like sequence on the viral RNA.
