**3. Etiology**

TBE is caused by TBEV, a small, neurotropic, lipid‐enveloped spherical RNA virus, the member of genus *Flavivirus*, family *Flaviviridae*. The viral RNA contains records for three structural (E (envelope), prM/M (precursor of membrane or membrane, respectively), and C (capsid)), and seven nonstructural viral proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5). Glycoprotein E is a major viral antigen and is associated with the production of neutralizing antibodies and the induction of protective immunity. It also plays a key role in the viral life cycle mediating the binding of virions to cell receptors and subsequent intraendosomal fusion [7].

TBEV occurs in three subtypes named as European, Siberian, and Far-Eastern subtype [1]. They are very closely related, both genetically and antigenically; variation in amino acids sequences between subtypes is 5–6% [8]. In spite of the pronounced genetic similarity of the subtypes the illness caused by individual subtype is not completely equivalent to those due to the other subtypes.

An important characteristic of the TBEV, which allows them alimentary route of infection, is their ability to maintain at least residual infectivity at acidic pH (above pH 1.42) [9]. TBEV maintains infectivity at very low environment temperatures (even below −70°C). On the contrary, it is heat labile; total inactivation of the virus occurs within 30 minutes at 56°C [10, 11]. It can be inactivated by pasteurization [12].
