Hijacked highways: plant virus modulation of vector proteins from entry to exit

Plant viruses rely on insect vectors to complete their transmission cycles, exploiting a diverse array of vector proteins to enable entry, intracellular movement, replication, and exit. This review synthesizes recent advances in our understanding of plant virus-vector protein interactions across noncirculative (NC) and circulative transmission modes, including vertical transmission. Key viral strategies include binding to surface proteins (e.g. Stylin-01, KRT), traversing epithelial barriers via receptor-mediated endocytosis (e.g. APN, ST6), trafficking through intracellular compartments (e.g. SNARE complexes, flotillin-2), and release through salivary exosomes. Some viruses hijack autophagy and apoptosis machinery to avoid degradation and ensure persistence. Others exploit reproductive proteins such as vitellogenin and sperm-specific serpin proteins - or even symbiont-derived membrane proteins - to achieve vertical transmission. In response, vectors activate immune pathways including RNA interference (RNAi), melanization, and mitogen-activated protein kinase signaling, although these defenses are frequently subverted by viral proteins. Mapping these molecular interactions highlights promising targets for intervention, including vector-targeted antibodies, RNAi-enabled symbionts, and receptor-blocking molecules. Together, these insights offer a path toward molecularly precise, ecologically sustainable strategies for disrupting plant virus transmission at the vector level.