[1] The TBEV genome is approximately 11kb in size, which contains a 5' cap, a single open reading frame with 3' and 5' UTRs, and is without polyadenylation.

[7] The immunogenicity of TBEV NS1 has been demonstrated, showcasing its ability to trigger oxidative stress and elicit the expression of immunoproteasome subunits.

This can occur at any part of the tick's life cycle but a horizontal transmission between infected nymphs and uninfected larvae co-feeding on the same host is thought to be key in maintaining the circulation of TBEV.

[5] TBEV envelope (E) proteins recognize heparan sulfate (and likely other receptors) on the host cell surface and are endocytosed via the clathrin mediated pathway.

Acidification of the late endosome triggers a conformational change in the E proteins, resulting in fusion, followed by uncoating, and release of the single-stranded RNA genome into the cytoplasm.

[12] Recognition causes the release of cytokines including interferons (IFN) α, β, and γ and chemokines, attracting migratory immune cells to the site of the bite.

Notably, tick saliva enhances infection by modulating host immune response, dampening apoptotic signals.

[12] The draining lymph node can also serve as a viral amplification site, from where TBEV gains systemic access.

IgG levels peak at about 6 weeks after the appearance of CNS symptoms, then decline slightly but do not dissipate, likely conferring life long immunity to the patient.

[1] However, in antigenic relatedness, based on the E, NS3, and NS5 proteins, all three sub-types are highly similar, and Louping Ill virus is the closest relative outside the collective TBEV group.

[21] Though the first description of what may have been TBE appears in records in the 1700s in Scandinavia,[13] identification of the TBEV virus occurred in the Soviet Union in the 1930s.

The expedition was led by virologist Lev A. Zilber, who assembled a team of twenty young scientists in a number of related fields such as acarology, microbiology, neurology, and epidemiology.

[22] The expedition returned in mid-August and in October 1937 Zilber and Sheboldova were arrested, falsely accused of spreading Japanese encephalitis.

As a consequence of the arrests, one of the important initial works was published under the authorship of expedition acarologist, Vasily S. Mironov.