TICK-BORNE ENCEPHALITIS VIRUS IGG PLUS ELISA

This Tick-borne encephalitis (TBE/FMSE) virus IgG plus antibody ELISA kit has been designed for the detection and the quantitative determination of specific IgG antibodies against Tick-borne encephalitis virus in human serum or plasma. The Plus ELISA contains an additional control protein, not present within our standard TBE/FMSE virus IgG antibody ELISA kit (ELS61239).

Microplates are coated with specific antigens to bind corresponding antibodies of the sample. After washing the wells to remove all unbound sample material a horseradish peroxidase (HRP) labelled conjugate is added. This conjugate binds to the captured antibodies. In a second washing step unbound conjugate is removed. The immune complex formed by the bound conjugate is visualized by adding Tetramethylbenzidine (TMB) substrate which gives a blue reaction product. The intensity of this product is proportional to the amount of specific antibodies in the sample. Sulphuric acid is added to stop the reaction. This produces a yellow endpoint colour. Absorbance at 450/620 nm is read using an ELISA microwell plate reader.

PRODUCT DETAILS – TICK-BORNE ENCEPHALITIS VIRUS IGG PLUS ELISA

• High sensitivity – 100%.
• High specificity – 100%.
• Short assay time – <3 hours.
• 1 x 96 tests.

BACKGROUND

Tick-borne encephalitis (TBE) virus is a flavivirus of the family Togaviridae. It is an enveloped single-stranded RNA virus with cubic icosahedral symmetry and ranges in size from 20-80nm in diameter. Three subtypes can be distinguished which show only little differences in their structural proteins. TBE virus is mainly transmitted by ticks (Ixodes ricinus, western subtype; Ixodes persulcatus, eastern subtype). The degree of contamination of ticks (and thus humans) in central Europe increases from west to east, and anybody may be affected. Specific antibody development yields a life-long immunity.

TBE is the most important tick-transmitted disease of man -beside Lyme disease, which is caused by the spirochete Borrelia burgdorferi. The clinical course of the disease depends on the immune status of the infected persons. A high virus production in the primary infected tissues is required for the passage of the blood-brain barrier and the resulting severe manifestations in the central nervous system.

REFERENCES

• Donoso Mantke, O.; Escadafal, C.; Niedrig, M.; Pfeffer, M.; Working Group For Tick-Borne Encephalitis Virus, C. (2011): Tick-borne encephalitis in Europe, 2007 to 2009. In Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin 16 (39).
• Mansfield, Karen L.; Horton, Daniel L.; Johnson, Nicholas; Li, Li; Barrett, Alan D. T.; Smith, Derek J. et al. (2011): Flavivirus-induced antibody cross-reactivity. In The Journal of general virology 92 (Pt 12), pp. 2821–2829.
• Roggendorf, M.; Heinz, F.; Deinhardt, F.; Kunz, C. (1981): Serological diagnosis of acute tick-borne encephalitis by demonstration of antibodies of the IgM class. In Journal of medical virology 7 (1), pp. 41–50.

THIS ELISA ASSAY IS FOR RESEARCH USE ONLY. IT IS NOT FOR USE IN DIAGNOSTIC PROCEDURES.