Abstract
Ferroptosis-like cell death in plants is a recently described mechanism triggered by iron accumulation and lipid peroxidation; however, its role in viral infection remains unclear. In this study, we investigated the effect of iron (Fe-EDTA) treatment on Nicotiana benthamiana plants infected with wild-type tomato bushy stunt virus (wtTBSV). Morphological and biochemical analyses under combined stress revealed pronounced symptoms, including growth inhibition, necrosis, leaf yellowing, chlorosis, and leaf deformation, while the expression of the viral suppressor protein P19 was reduced. Biochemical assays showed that low Fe-EDTA concentrations maintained the photosynthetic apparatus and increased chlorophyll content, whereas high concentrations induced lipid peroxidation and ferroptosis-like cell death. Our results suggest that excess iron activates RNA interference and ferroptosis-like death, thereby suppressing viral infection, while low iron concentrations preserve photosynthetic activity and alleviate symptoms. In addition, combined stress led to reduced levels of HSP70 and HSP90, indicating that iron homeostasis may interfere with cellular chaperones essential for viral replication. These findings highlight the key role of ferroptosis-like cell death in plant-virus interactions.