Tick-Borne Encephalitis Antibodies, Proteins & ELISA Kits

Tick-borne encephalitis (TBE) is a disease which affects the central nervous system (CNS) and it is caused by the neurotrophic tick-borne encephalitis virus (TBEV). TBE is endemic in European and Asian countries is predominantly transmitted through tick bites.

While 70-98% of TBE infections are asymptomatic, some individuals experience symptoms of headaches, fever, fatigue and nausea. This can progress to meningitis, meningoencephalitis, myelitis, encephalitis and mortality in extreme cases. 50% of people who acquire acute TBE infections develop post-encephalitic syndrome.

The main types of TBE vaccinations are based on inactivated whole viruses which have strains of both Far-Eastern and European subtypes of TBEV. While TBE vaccination is effective, there is still the need for further TBEV research to enhance and develop vaccines.

TBEV is composed of structural proteins such as capsid (C) proteins, envelope (E) glycoproteins, pre-membrane (preM) proteins and membrane (M) proteins. TBEV also consists of non-structural components; NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5. The C protein binds viral RNA, forming a nucleocapsid. PreM is responsible for preventing premature fusion of the E protein to the cell surface during viral exocytosis. PreM is cleaved into M protein which is responsible for causing E protein to rearrange and promote pathogenesis through cell binding, virion assembly and immunogenicity.

The TBEV E protein attaches to host cell receptors and receptor-mediated endocytosis occurs. Three host cell receptors have been suggested to bind to TBEV; glycosaminoglycan heparan sulfate (HS), human integrin αVβ3 and glucagon-like peptide-2 receptor (GLP2R).

At present, there is little research about how immune cell metabolism is affected by TBEV. Assay Genie provides a wide range of immunometabolism assays such as glycolysis, fatty acid oxidation, the citric acid (TCA) cycle and oxidative phosphorylation (OXPHOS) assays kits.

It has been shown that during the inflammatory response against TBEV, there is the production of interferon-alpha (IFN-alpha), IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1beta, IL-8 (CXCL8), IL-10, IL-12, IL-17A, IL-17F, IL-22, CCR5, CCL3, CXCL1, CXCL2 and CXCL10 (IP-10). It was also found that a Th1 immune response was indicative of a more severe form of TBE in comparison to Th17 and B cell responses.

Animal models are useful research tools which are often used in early stages of therapeutic drug development and pathogenesis studies. The main reservoirs of TBEV are ticks and small rodents. However, TBEV also infects domestic animals such as cats and dogs, birds, sheep and horses. Mice are suitable animal models for TBE infections as they mirror the symptoms experienced in humans and the physiopathological markers seen during TBE infection.

TBEV, Japanese Encephalitis Virus, Yellow Fever Virus, West Nile Virus, Zika virus and Dengue belong to the genus Flavivirus. Many studies have identified structural and genetic similarities between the Flavivirus viruses.

• West Nile Virus
• Yellow Fever Virus
• Japanese Encephalitis Virus
• Zika Virus