Tick-borne encephalitis causes

Tick-borne encephalitis is caused by a (+) ssRNA virus of the Flavivirus genus. Three subtypes of the virus exist including the Far East, European, and Siberian subtypes. The Ixodidae family of ticks is the primary vector associated with transmission, with other modes of transmission including the consumption of unpasteurized, raw milk.^[1] The virus itself is a member of the flavivirus genus with a (+) ssRNA genome enclosed in a capsid protein. The pathogenic process begins with the location of a host cell receptor. The virus is internalized through the process of endocytosis. During this time the virus hi-jacks the host cells replication machinery, in order to replicate many times within the host cell. Upon completion, the cell releases many immature virions for further progression of the disease.

• Member of the Falvivirus genus
• Flaviviridae family
• Three subtypes: Far East, European, and Siberian
• Viral strains are mostly homogeneous within infected European tick populations.
• Diversity exists within viral strains carried by Siberian and Far Eastern tick populations. Thus these populations host antigenic variations and a variety of subtypes.
• However the antigenic similarity within these populations allows for a generalized protection method among the different subtypes.^[2]

• (+)ssRNA genome enclosed in a capsid protein.
• Genome is protected by a lipid bilayer, provided by the host or target cell.
• Virus’s physical attributes include a spherical particle with an approximate diameter of 50-60nm.
• The genome lacks a 3′-poly(A) tail, yet provides a 5′ cap.
• In terms of length, the genome spans an average of 11kb.^[2]

• The Ixodidae family of hard ticks have been reported as the vector and reservoir of the Tick-borne encephalitis virus.
• Other modes of transmission include the consumption of raw milk as well as vertical transmission from mother to fetus.^[1]

• Virus replication commonly occurs within subcutaneous tissue.
• Dendritic cells transport the virus to the lymph nodes.
• The virus replicates at a high rate within the lymph nodes, further travelling into the bloodstream.
• Lymphocytes suffer great reductions due to infection with the regional lymph nodes.
• Further infection of external tissues occur within the viremic phase
• The later phase results in the infection of the CNS.
• Furthermore a host’s immune system will add to the severity of the infection, as resulting immune response includes inflammation CD8+ T-cells infiltrating the brain.
• Other immune responses such as the upregulation of proinflammatory cytokines increase the permeability of the blood-brain barrier.^[2]