This review examines how plant viruses cause disease by disrupting host cellular processes. Plant viruses are biotrophic pathogens requiring living tissue for replication. While some infections cause no symptoms or benefit the host, many trigger disease phenotypes through interference with host resources and cellular functions. The review highlights three major mechanisms of pathogenesis: (1) plant defence responses and their viral suppression, including hypersensitive response (HR) triggered by resistance genes and RNA silencing-mediated defenses disrupted by viral suppressors like the HCPro protein; (2) viral interference with host hormonal regulation, cell cycle control, and gene expression, exemplified by virus proteins interacting with auxin signaling and gibberellin biosynthesis pathways; and (3) effects on viral movement and cellular transport. The authors emphasize that disease symptoms result from complex interactions between induced plant defence mechanisms, viral counter-strategies, and co-option of host factors needed for viral replication. Recent evidence reveals interplay between plant development and antiviral defence signalling pathways, where interference at these intersections can trigger pathological manifestations independent of viral accumulation levels.

Key findings

• Plant viruses cause disease primarily through interference with host resources and disruption of cellular processes rather than direct toxicity, with symptom severity correlating with the number of affected genes
• Viral silencing suppressors like potyviral HCPro contribute to pathogenesis by interfering with RNA silencing pathways and disrupting microRNA-regulated developmental processes, sometimes causing symptoms without increasing viral accumulation
• Viral proteins interact with host regulatory proteins controlling hormones (auxin, gibberellins, ethylene), cell cycle progression, and gene expression, reprogramming host physiology to favor viral replication
• Plant resistance genes can trigger both localized hypersensitive response cell death and systemic necrotic symptoms that are independent phenomena, with disease manifestation depending on complex gene-to-gene interactions
• Mixed viral infections with complementary silencing suppressors produce synergistic severe symptoms, suggesting viral pathogens have evolved mechanisms to coordinately exploit host biology