Maybe such way: "Here, we report that tobacco plants infected with TMV exhibited an increase in HRF in two consecutive generations. ... Analysis of the response of the progeny of infected plants to TMV, Pseudomonas syringae, or Phytophthora nicotianae revealed a significant delay in symptom development. Infection of these plants with TMV or P. syringae showed higher levels of induction of PATHOGENESIS-RELATED GENE1 gene expression and higher levels of callose deposition." Palak et al., Plant Physiology August 2010 vol. 153 no. 4 1859-1870

Dear Alex, plant viruses are obligate intracellular parasites of plants and do need alive host cells in order to survive and reproduce themselves while bacterial pathogens are mostly intracellular phytoparasites that cause leakage of the electrolytes through modification of plant cell membranes, that leads to the accelerated death of host cells and necrotrophic nutrition of the bacteria after their invasion to the leaked cells. Pathogens abuse their hosts through deceiving their host defense systems. For example, A biotrophic pathogen that requires alive host cells to abuse them for its own nutrition and reproduction, induces jasmonic acid pathway against salicylic acid pathway, while the first leads to the defensive metabolites known to be effective against wound parasites, necrotrophic pathogens and insect pests but not biotrophic pathogens (rusts, powdery mildews, downy mildews, phytopathogenic protozoa, nematodes, viruses and some bacteria and Phytoplasmas). Vice verse, necrotrophic pathogens that have to kill host cells before eating and using their sources, change the metabolic balance biased for salicylic acid pathway that is effective against biotrophic pathogens. Then, it will not be so surprising to see such results You have found. With hemibiotrophic pthogens that indicate two phases of invasion, biotrophic then switched to vast necrotrophic invasion, we expect to see phase-dependent phenomena in this case according to the above-mentioned facts.

Thank you very much for your suggestion.

Now, I think that the virus interaction with host plant can interrupt the plant metabolic pathways/ receptors usually modified/used by the bacteria through T3SS or T4SS effectors, so bacteria cannot achieve usual benefits of their "weapons" application.

By the way, higher susceptibility to late blight and other diseases of virus-free potato plants was well known long time ago (but only for some viruses).