Abstract:Objective To clarify phyllosphere microbial responses to the invasion of areca palm velarivirus 1 (APV1), a virus causing yellow leaf disease of areca (Areca catechu), and provide a theoretical basis and technical support for the study of phyllosphere micro-ecology, exploration of excellent biocontrol resources, and green prevention and control of yellow leaf disease of areca.Methods We collected healthy leaves, mildly diseased leaves, and severely diseased leaves of areca. The phyllosphere microbial community structure and diversity were compared by high-throughput sequencing and bioinformatics methods. Furthermore, functional differences of phyllosphere microbial communities were analyzed.Results The dominant bacterial phyla in the phyllosphere of areca included Actinobacteriota, Proteobacteria, Acidobacteriota, Firmicutes, and Myxococcota, while the dominant fungal phyla were Ascomycota and Basidiomycota. As the disease became increasingly severe, bacterial richness initially increased then decreased while fungal richness initially decreased then increased. However, both bacterial diversity and fungal diversity showed a trend of first increasing and then decreasing. Firmicutes and Basidiomycota served as indicators of mildly diseased areca, with the relative abundance showing consistent trends with alpha diversity. The healthy plants and the diseased plants showed different phyllosphere microbial functions. Specifically, the environmental information processing function was significantly higher in severely diseased areca plants than in healthy ones. Additionally, the relative abundance of symbiotroph fungi in the phyllosphere were significantly higher in severely diseased areca plants than in healthy ones.Conclusion The yellow leaf disease significantly alters the phyllosphere microbial community structure and diversity of areca, with greater changes during the early disease stage. This suggests that areca may defend against APV1 infection by recruiting beneficial microorganisms, regulating cellular metabolism and biochemical reactions, and activating autoimmunity.