Programmed cell death (PCD) pathways caused by Turnip mosaic virus (TuMV) infection before symptom appearance were studied by light microscopy and electrolyte leakage following sap inoculation of Brassica carinata (Ethiopian mustard) TZ-SMN-44-6 plants. Leaf responses to inoculation with avirulent (TuMV-avir) and virulent (TuMV-vir) isolates, and mock-inoculation, were compared at 2, 20 and 52 h after inoculation (hai). The phenotypes induced were localized resistance (TuMV-avir) and systemic susceptibility (TuMV-vir). No visible TuMV symptoms were recorded in any inoculated plants during the 2–52 hai sampling period, but appeared as chlorotic spots in inoculated leaves at 5 days after inoculation. With TuMV-vir alone, they were followed by systemic infection (mosaic). Dead cell number, deformation, percentage area and percentage integrated intensity, and conductivity of electrolyte leakage data, were analysed to examine their possible roles in stimulating cell death pathways. At 2 hai, dead cell number and percentage area were significantly greater for TuMV-avir than TuMV-vir infection or mock-inoculation. Overall, isolate TuMV-vir caused significantly greater cell deformation than TuMV-avir, whereas wounding by mock-inoculation had negligible effects. By 52 hai, isolate TuMV-avir caused significantly greater electrolyte leakage than isolate TuMV-vir or mock-inoculation. This suggests both isolates triggered morphological changes consistent with apoptotic-like PCD and necrosis-like PCD that depended upon isolate virulence and stage of infection, respectively. These findings highlight how quantification of dead cell deformation and electrolyte leakage offer a new understanding of compatible and incompatible plant responses to early virus infection in plants.