Plant viruses, as obligate intracellular parasites, induce significant changes in the cellular physiology of host cells to facilitate their multiplication. These alterations often lead to the development of symptoms that interfere with normal growth and development, causing USD 60 billion worth of losses per year, worldwide, in both agricultural and horticultural crops. However, existing literature often lacks a clear and concise presentation of the key information regarding the mechanisms underlying plant virus-induced symptoms. To address this, we conducted a comprehensive review to highlight the crucial interactions between plant viruses and host factors, discussing key genes that increase viral virulence and their roles in influencing cellular processes such as dysfunction of chloroplast proteins, hormone manipulation, reactive oxidative species accumulation, and cell cycle control, which are critical for symptom development. Moreover, we explore the alterations in host metabolism and gene expression that are associated with virus-induced symptoms. In addition, the influence of environmental factors on virus-induced symptom development is discussed. By integrating these various aspects, this review provides valuable insights into the complex mechanisms underlying virus-induced symptoms in plants, and emphasizes the urgency of addressing viral diseases to ensure sustainable agriculture and food production.

Plant viruses pose a significant threat to global agriculture, leading to substantial crop losses that jeopardise food security and disrupt ecosystem stability. These viral infections often reprogramme plant metabolism, compromising key pathways critical for growth and defence. For instance, infections by cucumber mosaic virus alter amino acid and secondary metabolite biosynthesis, including flavonoid and phenylpropanoid pathways, thereby weakening plant defences. Similarly, tomato bushy stunt virus disrupts lipid metabolism by altering the synthesis and accumulation of sterols and phospholipids, which are essential for viral replication and compromise membrane integrity. Recent advancements in gene‐editing technologies, such as CRISPR/Cas9, and metabolomics offer innovative strategies to mitigate these impacts. Precise genetic modifications can restore or optimise disrupted metabolic pathways, enhancing crop resilience to viral infections. Metabolomics further aids in identifying metabolic biomarkers linked to viral resistance, guiding breeding programmes aimed at developing virus‐resistant plants. By reducing the susceptibility of crops to viral infections, these approaches hold significant potential to reduce dependence on chemical pesticides, increase crop yields and promote sustainable agricultural practices. Future research should focus on expanding our understanding of virus–host interactions at the molecular level while exploring the long‐term ecological impacts of viral infections. Interdisciplinary approaches integrating multi‐omics technologies and sustainable management strategies will be critical in addressing the challenges posed by plant viruses and ensuring global agricultural stability.

Southern tomato amalgavirus (STV) is a cryptic pathogen that is abundant in tomato production fields and intensifies the resurgence of tomato yellow stunt disease (ToYSD), together with other phytoviruses. Here, we mapped the geographical and genomic diversity, phylogenetics, and evolutionary dynamics of STV. We found that STV prevailed across China and Pakistan, with a maximum average rate of infection of 43.19% in Beijing, China, and 40.08% in Punjab, Pakistan. Subsequently, we amplified, cloned, and annotated the complete genome sequences of STV isolates from Solanum lycopersicum L. in China (OP548653 and OP548652) and Pakistan (MT066231) using Sanger and next-generation sequencing (NGS). These STV isolates displayed close evolutionary relationships with others from Asia, America, and Europe. Whole-genome-based molecular diversity analysis showed that STV populations had 33 haplotypes with a gene diversity (Hd) of 0.977 and a nucleotide diversity (π) of 0.00404. The genetic variability of RNA-dependent RNA-polymerase (RdRp) was higher than that of the putative coat protein (CP) p42. Further analysis revealed that STV isolates were likely to be recombinant but with a lower-to-moderate level of confidence. With a variable distribution pattern of positively and negatively selected sites, negative selection pressure predominantly acted on p42 and RdRp. These findings elaborated on the molecular variability and evolutionary trends among STV populations across major tomato-producing regions of the world.

Rice black-streaked dwarf virus (RBSDV) is the main pathogen causing maize rough dwarf disease (MRDD) in China. Typical enation symptoms along the abaxial leaf veins prevail in RBSDV-infected maize inbred line B73 (susceptible to RBSDV), but not in X178 (resistant to RBSDV). Observation of the microstructures of epidermal cells and cross section of enations from RBSDV-infected maize leaves found that the increase of epidermal cell and phloem cell numbers is associated with enation formation. To identify proteins associated with enation formation and candidate proteins against RBSDV infection, comparative proteomics between B73 and X178 plants were conducted using isobaric tags for relative and absolute quantitation (iTRAQ) with leaf samples at the enation forming stage. The proteomics data showed that 260 and 316 differentially expressed proteins (DEPs) were identified in B73 and X178, respectively. We found that the majority of DEPs are located in the chloroplast and cytoplasm. Moreover, RBSDV infection resulted in dramatic changes of DEPs enriched by the metabolic process, response to stress and the biosynthetic process. Strikingly, a cell number regulator 10 was significantly down-regulated in RBSDV-infected B73 plants. Altogether, these data will provide value information for future studies to analyze molecular events during both enation formation and resistance mechanism to RBSDV infection.