Page 92 - TBE_Book_V2_2019

Chapter 4

Pathogenesis of TBE

with a focus on molecular mechanisms

Andrea Kröger and Anna K. Överby
Key Points

• In this chapter we describe the pathogenesis of tick-borne encephalitis virus (TBEV).

• To cause infection, TBEV needs to cross three different barriers; the physical, the innate and
adaptive, and the blood-brain barrier.
• The trigger of innate immune and adaptive immune responses, by TBEV is necessary to clear the
infection.
• TBEV employs strategies to evade the innate immune response.

• Tools to study TBEV pathogenicity such as mouse knock-out models and reverse genetics are also
discussed.

Overcoming the barriers of the the skin, mucosal membranes, and stomach.
However, this first barrier to TBEV is already
host overcome by the tick through direct injection
of the virus into the skin of the host during
The host has highly effective defense
blood feeding. This allows the first replication
mechanisms against infections (Figure 1). The phase of the virus locally in the skin. The
overwhelming majority of infections are second barrier is the coordinated innate and
normally blocked by physical barriers such as

Figure 1: Barriers of TBEV infection

Host barriers prevent or repel infection by microbes. Anatomical and chemical barriers, cell-intrinsic and
cellular-innate immune response, adaptive immunity and other barriers have to be bypassed by invading
viruses to establish viral replication, spread and neuroinvasion. TBEV overcome the skin as anatomical barrier
by transfer through a tick bite. The complement system as well as innate and adaptive immune response
inhibit viral replication and spread. How the virus mediates neuroinvasion is still unknown, but the virus passes
through CNS barriers.

87