Tick-borne encephalitis: causes and pathogenesis

Causes of tick-borne encephalitis

Tick-borne encephalitis is caused by tick-borne encephalitis virus belonging to the Flaviviridae family . A virus with a size of 45-50 nm consists of a nucleocapsid with a cubic type of symmetry and is coated with a shell. Nucleocapsid contains RNA and protein C (core). The envelope consists of two glycoproteins (membrane M, shell E) and lipids. Based on the analysis of the homology of the gene fragment encoding the E protein, five main genotypes of the virus are isolated:

• genotype 1 - Far Eastern variant;
• genotype 2 - Western (Central European) variant;
• genotype 3 - Greek-Turkish variant;
• genotype 4 - the East Siberian variant;
• genotype 5 - Ural-Siberian variant.

Genotype 5 - the most common, found in most of the area of the tick-borne encephalitis virus.

The virus of tick-borne encephalitis is cultivated in chick embryos and cultures of tissues of various origins. With prolonged passage, the pathogenicity of the virus is reduced. Among laboratory animals, white mice, rat suckers, hamsters and monkeys are most susceptible to infection with the virus, among the domestic animals are sheep, goats, pigs, horses. The virus is unequally resistant to various environmental factors: it boils for 2-3 minutes during boiling, it breaks easily during pasteurization, treatment with solvents and disinfectants, but it is capable of long-term viability at low temperatures and in a dried state. The virus survives long enough in such foods as milk or oil, which can sometimes be sources of infection. The virus is resistant to the action of low concentrations of hydrochloric acid, so the food path of infection is possible.

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Pathogenesis of tick-borne encephalitis

After introduction, the virus multiplies locally in skin cells. Degenerative-inflammatory changes develop on the site of the bite in the tissues. With the alimentary route of infection, virus fixation occurs in the epithelial cells of the gastrointestinal tract.

The first wave of viralemia (transient) is caused by the penetration of the virus into the blood from the sites of primary localization. At the end of the incubation period, a second wave of viremia occurs, coinciding with the onset of the virus multiplication in the internal organs. The final phase is the introduction and replication of the virus in the cells of the central nervous system and the peripheral nervous system.

"Plus-stranded" RNA of tick-borne encephalitis virus can directly translate genetic information to the ribosomes of the sensitive cell, i.e. Perform mRNA functions.

The virus of tick-borne encephalitis in the central nervous system mainly affects the gray matter, resulting in the development of polyoencephalitis. The observed lesions are nonspecific and include cellular inflammation, hyperplasia, glial proliferation, and necrosis of neurons.

The progredient forms of tick-borne encephalitis are associated with the long-term retention of the virus in active form in CNS cells. In the development of persistent infection, a significant role is assigned to the mutant forms of the virus.

Pathomorphology of tick-borne encephalitis

With microscopy of the brain and membranes, they exhibit hyperemia and edema, infiltrates from mono- and polynucleated cells, mesodermal and glial reactions. Inflammatory-degenerative changes in neurons are localized mainly in the anterior horns of the cervical segments of the spinal cord, the nuclei of the medulla oblongata, the bridge of the brain, and the cerebral cortex. Characteristic destructive vasculitis with necrotic foci and puncture hemorrhages. For the chronic stage of tick-borne encephalitis fibrotic changes in the shells of the brain are typical with the formation of adhesions and arachnoid cysts, marked proliferation of glia. The most severe, irreversible lesions occur in the cells of the anterior horns of the cervical segments of the spinal cord.