**4. Conclusion**

diffuse and focal perivascular infiltrates and proliferates to a small or virtually absent cellu‐ lar inflammation is associated with the virulence of the virus strains and to a large extent with the immunological reactivity of the organism to infection. In assessing the nature of the pathological process, we stand in solidarity with Yerman, concluding that the immunopa‐ thology of tick-borne encephalitis includes both immediate type hypersevsitivity, and de‐ layed-type hypersevsitivity, a different combination of which creates the impression of

Cerebral symptoms +++ +/++ - Focal neurological symptoms ++ +++ -

The current of disease heavy heavy / moderate

The during the onset of death, week the first week 2-3-4 weeks Till one week

Alteration of neurons +++ ++/+++ +/± Gemocirculating disorders +++ ++/+++ ±/-

neutrophils ++ + ±/ lymphocytes/ histiocytes +/++ ++/+++ ++

focal ++ ++/+++ +/± diffuse ++ ++/+++ - Reactions of ITH +++ ±/+ - Reactions of DTH ±/+ ++/+++ +/±

Note: + + + pronounced, + + moderate severity, + weak expression, ± low intensity, - the lack of symptom/sign.

**Table 3.** Clinical and morphological variants of tick-borne encephalitis

**Clinical and morphological variants of the disease The first The second The third**

> 2 weeks. -56.6% 3 weeks. - 13.4% 4 weeks. - 30%

light, with or without clinical picture

no

different types of inflammatory reaction.

Mortality 100 %

**Indexes**

136 Encephalitis

*The clinical picture*

*The morphological picture*

Infiltration due to:

Proliferation of glia:

On the basis of their own and literature data is given the modern interpretation of the patho‐ morphology of tick-borne encephalitis (TBE) in terms of immunopathological nature of the inflammation. It is shown that the pathological picture of central nervous system reflects the hyperergic nature of inflammation with TBE. In the morphogenesis of the pathological proc‐ ess traced the consistent development of immediate type hypersensitivity reactions, initiated by the damaging effect of the virus in brain tissue, and delayed type hypersensitivity reac‐ tions to ensure the formation of local (tissue) immunity. For a comprehensive assessment of pathology of tick-borne encephalitis in humans and experimental animals set the variability of its manifestations, this depends on the properties of the infecting virus strain, such as the virus-induced immune response and the stage of disease morphogenesis. On this basis, div‐ ided into three clinical and morphological variant manifestations of infection with TBEV.
