Page 166 - TBE_Book_V2_2019

Chapter 9

Immunology of

TBEV infection

Sara Gredmark-Russ and Renata Varnaite

Key Points

• Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by
the tick-borne encephalitis virus (TBEV).

• TBE is usually a biphasic disease and in humans the virus can only be detected during the first
(unspecific) phase of the disease.
• Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated
tissue damage of the central nervous system may contribute to the natural course of TBE.
• The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse
models.
• Characterization of human immune responses to TBEV is primarily conducted in peripheral blood
and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection.
• Natural killer (NK) cells and T cells are activated during the second (meningoencephalitic) phase
of TBE. The potential involvement of other cell types has not been examined to date.
• Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells,
infiltrate into the cerebrospinal fluid of TBE patients.

Introduction

The immune system is a complex network of gen due to its ability to generate immuno-
organs and processes within the host which logical memory. Importantly, the innate and
protects from the invasion of pathogenic adaptive immune systems function as allies to
microorganisms. This network consists of an produce a more efficient total response than
enormous variety of cells and molecules with either one alone.
specialized functions and is generally divided Tick-borne encephalitis (TBE) is a viral
into innate and adaptive immunity. The innate infectious disease of the central nervous
immune system provides the first line of
system (CNS) caused by tick-borne
defense in infection and acts broadly against
encephalitis virus (TBEV). It is usually a
various pathogens, whereas the adaptive biphasic disease manifesting with influenza-
immune system generates a highly specialized like febrile illness during the first (viremic/
response to individual pathogens. Adaptive
febrile) phase followed by a second (meningo-
immunity is also capable of “striking” harder
encephalitic) phase with neurological symp-
upon secondary exposure to the same patho-

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