The probable reason is that ozone targets inflammatory mechanismsby acting on more intricate intracellular pathways to modulate the interactionbetween nuclear factor erythroid-2-related factor 2/nuclear factor-κB (orNrf2/NF-κB) and the mitochondria-associated inflammasome NOD-like receptorthermal protein domain associated protein 3 (or NLRP3), which in turn leads toreductions in serum inflammatory markers, whose role in viral diseases and otherinflammatory conditions has been extensively documented[44,45]. This evidence concerns the gene NLRP3 and viral load.