The differences observed between our data and those in literature could suggest a different role of salicylic acid in TYLCSV infection but they could also be explained considering that. Autophagy is an evolutionarily conserved mechanism for intracellular recycling whereby large protein complexes and aggregates, organelles, and even invading pathogens are encapsulated in specific vesicles called autophagosomes, which are then engulfed and digested by vacuoles/lysosomes. This process is essential for tissue homeostasis and development, TAPI-0 and plays a critical role in the ability of plants to survive nutrient starvation as well as to exposure to abiotic and biotic stresses. The analysis of overrepresented functional categories highlighted a significant enrichment of autophagy-related transcripts among the genes up-regulated during the TYLCSV/tomato compatible interaction. All these transcripts were related to the formation of autophagosomes. In particular, several transcripts coding for isoforms of ATG8, key regulator and marker of the autophagic process, were induced during infection. ATG8 is an ubiquitin-like protein required for the formation of autophagosomal membranes. During the autophagic process, ATG8 anchors to the autophagosomes membranes by a carboxyl terminal phosphatidylethanolamine lipid. Interestingly, activation of ATG8 genes was also observed in Arabidopsis infected by CabLCV. Other TYLCSV-induced transcripts coded for ATG9, involved in the membrane delivery to autophagosomes, and ATG12, an ubiquitin-like protein involved in the formation of the ATG8-PE complex. Being intracellular parasites, viruses deal with the autophagic machinery during the infection process. In this respect, autophagy can play both anti-viral and pro-viral roles in viral life cycle and pathogenesis. On one hand, autophagy proteins can target viral components for lysosomal degradation and play a role in initiating immune response to infection. In this context, we can suppose that the observed up-regulation of autophagy genes is a host attempt to counteract viral invasion by elimination of exogenous viral particles. On the other hand, some animal viruses are able to hijack autophagy to foster their intracellular growth. In plants it is known that virus multiplication sequesters important cellular components, TAPI-2 causing cell starvation and activation of genes involved in programmed cell death. Cell death would be detrimental to viruses, in particular those like TYLCSV, which are restricted to a few cells in the phloem. Activation of autophagy by negatively regulating PCD, would prevent cells to die, thus maintaining a favourable environment for the virus. Clinical and experimental results have shown that the peripheral analgesic efficacy of opioids is enhanced in the presence of inflammation and tissue injury. The mechanisms responsible for this phenomenon involves the following events: increases in the opioid receptor mRNA level and opioid receptor expression level, an increase in the axonal transport and accumulation of these receptors in the peripheral sensory nerve endings, and an increase in the opioid agonist binding to their corresponding receptor. Moreover, inflammation induces the release of endogenous opioid peptides. Studies investigating the molecular mechanisms involved in the enhanced effects of opioid treatments in the periphery caused by inflammation mainly focus on the m-opioid receptor and the chronic inflammatory processes. Inflammation enhances the axonal transport of opioid receptors toward the periphery, which is preceded by an increase in opioid receptor mRNA transcription.