Areca palm velarivirus 1 encoded CP suppresses antiviral RNA silencing by mediating the autophagic degradation of SGS3 and disrupting the SGS3-RDR6 interaction.

Abstract

Areca palm velarivirus 1 (APV1) is the causative agent of yellow leaf disease (YLD), leading to severe yield losses in areca palms. However, how APV1 counteracts host immunity remains largely underexplored, and the underlying mechanisms are still poorly understood. RNA silencing is an evolutionarily conserved antiviral defense mechanism in eukaryotes. In this study, we identify the APV1-encoded capsid protein (CP) as a viral suppressor of RNA silencing (VSR) that inhibits both local and systemic silencing triggered by single-stranded RNA (ssRNA). Mechanistically, CP interacts with host Suppressor of Gene Silencing 3 (AcSGS3), a key component of the RNA silencing pathway, and promotes its degradation via autophagy. Additionally, CP disrupts the SGS3-AcRDR6 (RNA-dependent RNA polymerase 6) interaction, impairing the RNAi signaling cascade. Our findings reveal a novel dual mechanism to counteract host RNA silencing in which APV1 CP disrupts the SGS3-AcRDR6 complex and exploits the autophagic pathway to degrade AcSGS3, thereby undermining host antiviral defenses.