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Chapter 9: Immunology of TBEV infection

Sweden measured seroprevalence for TBEV in tissue damage, but the exact mechanism is
an endemic area and found that only 25% of unclear. More research is needed in order to
individuals who were seropositive for TBEV fully understand the development of TBE in
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developed clinical TBE. order to create effective and specific
therapeutic strategies.
Clinical appearance and the progression of
TBE may also be related to host genetic
Acknowledgements: SGR is supported by the
factors. Studies on TBE in this context have
Marianne and Marcus Wallenberg Foundation.
thus far not been able to correlate We sincerely thank Servier Medical Art (http://
susceptibility to TBE or disease severity to one smart.servier.com/) for providing high-quality
single host genetic factor, but a few graphics, which we modified and compiled to
candidates have been suggested including create the figures for this chapter of the book.
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CCR5Δ32 polymorphism, a functional TLR3
receptor, 34-36 5 different SNPs in the interferon
-induced antiviral proteins oligoadenylate Contact: sara.gredmark.russ@ki.se
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synthetase 2 (OAS2) and 3 (OAS3), 2 SNPs in
the promoter region of CD209 (encoding
Citation: Gredmark-Russ S, Varnaite R.
dendritic cell-specific intercellular adhesion
molecule (ICAM)-3 grabbing non-integrin (DC- Immunology of TBEV infection. Chapter 9. In:
SIGN)) expressed on the surface of dendritic Dobler G, Erber W, Bröker M, Schmitt HJ: The
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cells, and SNPs in interleukin 28B (IL28B) and TBE Book. 2nd ed. Singapore: Global Health
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interleukin 10 (IL10). In a more recent study, Press; 2019. doi: 10.33442/978-981-14-0914-
1_9
the rs17576 SNP in the MMP-9 gene
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predisposed TBE patients for CNS damage.
References

Conclusions 1. Lindquist L, Vapalahti O. Tick-borne
encephalitis. Lancet. 2008;371:1861-71.
TBE is a complex and rather understudied
2. Holzmann H. Diagnosis of tick-borne
disease in the context of human immune encephalitis. Vaccine. 2003;21 Suppl 1:S36-40.
system responses. In vitro experiments,
animal models, as well as research in humans 3. Gelpi E, Preusser M, Garzuly F, Holzmann H,
Heinz FX, Budka H. Visualization of Central
have greatly contributed to describing TBEV
European tick-borne encephalitis infection in
infection and defining the mechanism of TBE
fatal human cases. J Neuropathol Exp Neurol.
disease progression, however, many aspects 2005;64:506-12.
of it remain to be investigated further.
4. Gelpi E, Preusser M, Laggner U, et al.
It is clear that TBEV is a potent inducer of Inflammatory response in human tick-borne
innate immunity, but at the same time the encephalitis: analysis of postmortem brain
virus is capable of antagonising certain tissue. J Neurovirol. 2006;12:322-7.
pathways of innate immune responses. 5. Nestle FO, Di Meglio P, Qin JZ, Nickoloff BJ. Skin
Adaptive immune system responses are also immune sentinels in health and disease. Nat
initiated during TBE as reflected by anti-TBEV Rev Immunol. 2009;9:679-91.
antibody presence in serum, as well as NK and
6. Kazimirova M, Thangamani S, Bartikova P, et al.
T cell activation in peripheral blood of TBE Tick-Borne Viruses and Biological Processes at
patients. Local pathogenesis in the central
the Tick-Host-Virus Interface. Front Cell Infect
nervous system in TBE may be attributed to Microbiol. 2017;7:339.
both direct viral effects and immune mediated

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