In animal experiments, CXCR2 signaling contributes to the neutrophil migration from the bone marrow into blood under stress stimuli [62] and IL-22 causes neutrophilia mediated by CXCL1 release from hepatocytes [37, 43], and similar mechanisms could play a role in neutrophil mobilization and migration in TBE patients, contributing to a viral spread within infected cells. Here, CXCR2 is linked to tick-borne encephalitis.