Plant viruses are tiny pathogenic obligate parasites that cause significant damage to global crop production. They exploit and manipulate the cellular components of host plants to ensure their own survival. In response, plants activate multiple defense signaling pathways, such as gene silencing and plant hormone signaling, to hinder virus propagation. Growing evidence suggests that the regulation of protein homeostasis plays a vital role in the ongoing battle between plants and viruses. The ubiquitin-proteasome-degradation system (UPS) and autophagy, as two major protein-degradation pathways, are widely utilized by plants and viruses in their arms race. One the one hand, these pathways act as essential components of plant’s antiviral defense system by facilitating the degradation of viral proteins; on the other hand, viruses exploit the UPS and autophagy to create a favorable intracellular environment for viral infection. This review aims to provide a comprehensive summary of the events involved in protein homeostasis regulation during viral infection in plants. Gaining knowledge in this area will enhance our understanding of the complex interplay between plants and viruses.

Summary: Plant viruses often suppress jasmonic acid (JA)‐mediated defences through disturbing JA signalling or biosynthesis pathways to benefit their own infection. Few studies have examined how the precursors of JA biosynthesis are regulated by viral infection. In this study, we demonstrate that rice black‐streaked dwarf virus (RBSDV) infection inhibits the production of α‐linolenic acid (C18:3), a key JA biosynthesis precursor that is catalysed by a set of fatty acid desaturases (FADs). The viral capsid protein P10 directly interacts with OsFAD7, an ω‐3 fatty acid desaturase, and promotes its autophagic degradation through an ATG8‐interaction motif (AIM). This disrupts JA production and weakens antiviral defence against RBSDV infection. Genetic analysis reveals that overexpression of OsFAD7 enhances JA levels and resistance to virus. But OsFAD7‐mediated antiviral resistance is attenuated if OsCOI1a, a JA receptor, is silenced, indicating that the enhancement of resistance to RBSDV infection conferred by OsFAD7 depends on the JA pathway. Our findings reveal a novel viral strategy that suppresses JA biosynthesis at its metabolic source, providing insights for developing viral protection strategies and virus‐resistant crops.