In its natural habitat, TBEV is maintained by transmission between infected and non-infected ticks when they co-feed on small forest animals [6] [7] [8] . Humans are incidental hosts for ticks and may become infected by a feeding infected tick. The clinical manifestations caused by TBEV range from inapparent infections and fevers, with complete recovery of patients, to debilitating or fatal encephalitis. The proportion of fatal human infections varies widely in different regions and in different years. The factors that determine disease severity are poorly defined but correlations between viral subtype and disease severity have been described. TBEV strains are currently divided into 3 closely related subtypes, i.e. western-European (WE), Siberian (SIB) and Far Eastern (FE) [9] . FE TBEV is recognised as the most virulent pathogen with a 20-40% case fatality rate. The SIB subtype is considered less virulent (7-8% case fatality rate) but chronic disease occurs more frequently (1-3%) . Western European strains are the least virulent with case fatality rates lower than 2%. However, a range of clinical manifestations, from asymptomatic to encephalitic is observed for all TBEV subtypes [1, 2] and the underlying basis for this has not yet been adequately explained.