Research reveals that viral protein P25 interacts with eIF4E, enhancing its role in 3′-CITE-mediated translation in Areca palm Velarivirus 1.
Abstract Plant viruses employ diverse strategies to hijack host machinery for viral translation initiation. 3′ cap-independent translation enhancers (3′-CITEs) have been identified in many members of the families Tombusviridae and Luteoviridae. However, viral proteins that regulate 3′-CITE-mediated translation remain unreported, and the underlying mechanisms are still poorly understood. Closteroviruses are important pathogens that infect many economically significant crops, yet their modes of translation initiation remain largely unexplored. Areca palm velarivirus 1 (APV1), a member of the Closteroviridae family, is the causative agent of yellow leaf disease (YLD) in areca palms. Here, we demonstrate that eukaryotic initiation factor 4E (eIF4E) specifically binds to the 3′-UTR of APV1. The viral protein P25, encoded by APV1, interacts with eIF4E, enhances its stability, alters its subcellular localization, and promotes its recruitment to APV1 virions. Notably, P25 significantly enhances cap-independent viral translation. We identify the 3′-UTR of APV1 as the first reported 3′-CITE in the Closteroviridae family. Our study reveals P25 as the first viral regulator of 3′-CITE-mediated translation initiation, providing new insights into the molecular mechanisms of viral infection.
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Wan et al. (2025) studied this question.
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