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The Tick-borne encephalitis virus (TBEV) envelope protein (E protein) is the primary structural component on the surface of the virion and serves as the major antigen for the host immune response (UniProt P08486). It belongs to the class II viral fusion proteins and is responsible for mediating viral attachment to host cell receptors and subsequent membrane fusion within the endosome (PubMed: 29466770). As the principal target for neutralizing antibodies, the E protein is the central component of all currently licensed inactivated TBE vaccines, such as FSME-IMMUN and Encepur (WHO). The protein undergoes significant conformational changes during the infection process, transitioning from a dimer to a trimer to facilitate fusion (PubMed: 11160722). Mutations or variations in the E protein can influence viral virulence and the effectiveness of cross-protection between different TBEV subtypes, including European, Siberian, and Far Eastern strains. Therapeutic strategies targeting this protein focus on preventing viral entry into the central nervous system, thereby mitigating the risk of severe neurological disease (PubMed: 33467517).
Induction of neutralizing antibodies that bind to the E protein, preventing viral attachment to host receptors and inhibiting the pH-dependent membrane fusion required for viral entry.
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