In inflammation, including the observed TBEV infection and bacterial co-infections, Nrf2 activation ultimately restores redox homeostasis by upregulating essential antioxidants, including heme oxygenase 1 (HO-1), which is known to be a component of effective TBE cell resistance to numerous pathogens [44], but also superoxide dismutase and thioredoxin reductase. This evidence concerns the gene HMOX1 and tick-borne encephalitis.