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Anti-Epstein-Barr Virus IgG Avidity ELISA kit (VCA) is a Indirect ELISA kit for the measurement of Anti-Epstein-Barr Virus IgG Avidity (VCA) in Human in Citrate plasma, Heparin Plasma, Serum samples.

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Key facts

Detection method
Colorimetric
Sample types
Citrate plasma, Heparin Plasma, Serum
Assay type
Indirect
Reactive species
Human

Reactivity data

Application
ELISA
Reactivity
Reacts
Dilution info
-
Notes

-

What's included?

1 x 96 Tests
Components
20X Washing Solution
1 x 50 mL
Bottle
1 x 1 Unit
Cover foil
1 x 1 Unit
Epstein Barr virus (IgG) Coated Microplate (12 x 8 wells)
1 x 1 Unit
Epstein Barr virus anti-IgG HRP Conjugate
1 x 20 mL
Epstein-Barr Virus (VCA) IgG Control High
1 x 2 mL
Epstein-Barr Virus (VCA) IgG Control Low
1 x 2 mL
Epstein-Barr Virus IgG Cut-off Control
1 x 3 mL
Epstein-Barr Virus IgG Negative Control
1 x 2 mL
Epstein-Barr Virus IgG Positive Control
1 x 2 mL
IgG Sample Diluent
1 x 100 mL
Reagent
1 x 15 mL
Stop Solution
1 x 15 mL
Strip holder
1 x 1 Unit
TMB Substrate Solution
1 x 15 mL

Recommended products

Anti-Epstein-Barr Virus IgG Avidity ELISA kit (VCA) is a Indirect ELISA kit for the measurement of Anti-Epstein-Barr Virus IgG Avidity (VCA) in Human in Citrate plasma, Heparin Plasma, Serum samples.

Key facts

Detection method
Colorimetric
Sample types
Citrate plasma, Heparin Plasma, Serum
Assay type
Indirect
Reactive species
Human
Assay Platform
Pre-coated microplate (12 x 8 well strips)

Storage

Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
Multi
Storage information
Please refer to protocols

Notes

The Anti-Epstein-Barr Virus IgG ELISA (Enzyme-Linked Immunosorbent Assay) kit (VCA) (ab222940) is designed for the qualitative determination of Epstein-Barr virus viral capsid (VCA)-specific IgG avidity in human serum or plasma (citrate, heparin) to differentiate between acute and past infection.

Microplates are coated with specific antigens to bind the corresponding antibodies of the sample (dual pipetting). After washing the wells to remove all unbound sample material, one well is incubated with reagent and the corresponding well with washing buffer. The reagent removes the low-avidity antibodies from the antigens whereas the high-avidity ones are still bound to the specific antigens. After a second washing step to remove the rest of reagent and low-avidity antibodies, a horseradish peroxidase (HRP) labeled conjugate is added. This conjugate binds to the captured antibodies. In a third 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 specimen. Sulphuric acid is added to stop the reaction. This produces a yellow endpoint color.

Absorbance at 450/620 nm is read using an ELISA microwell plate reader.

The presence of IgG antibodies to Epstein-Barr Virus indicates the occurrence of the infection but does not distinguish between recent and past infection. Specific IgM antibodies are first detected approximately in ten days and peak at about four weeks post infection. They may persist for several months after acute infections. Based on the evidence that antibody avidity gradually increases after exposure to an immunogen, avidity of IgG antibodies can be used as a marker for distinguishing recent primary from long-term infections. Avidity describes the binding strength of a specific antibody to its antigen. Low-avidity IgG antibodies indicate a primary infection, whereas the presence of IgG antibodies with high avidity points to persistency or reactivation of infection.

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.
Activity summary

Immunoglobulin G (IgG) often referred to as IgG is the most common type of antibody found in blood circulation. It is an important element of the immune response enabling the body to identify and neutralize pathogens such as bacteria and viruses. IgG antibodies have a molecular weight of approximately 150 kDa. They are produced by B cells and are distributed predominantly in blood and extracellular fluid allowing them to play a significant role in immunity. IgG antibodies come in four subclasses: IgG1 IgG2 IgG3 and IgG4 each differing in their heavy chain structure and effector functions.

Biological function summary

IgG antibodies function as an important component of the adaptive immune system. They form part of complex immune responses where they help in antigen recognition and neutralization. These antibodies can opsonize pathogens making them more recognizable to phagocytes for destruction. IgG also activates the complement system which contributes to the lysis of pathogenic cells. As a bridge between innate and adaptive immunity IgG mediates the interaction with natural killer (NK) cells enhancing the cell-mediated immune response.

Pathways

The signaling pathways involving IgG antibodies include the classical complement pathway and Fc receptor signaling. The classical complement pathway complements the antibodies in opsonizing pathogens promoting inflammation and leading to the lysis of pathogens. Fc receptors on immune cells recognize and bind to the Fc region of IgG triggering phagocytosis and the cytotoxic activity of immune effector cells. IgG is related to other proteins such as complement proteins and Fcγ receptors which are essential for its role in immune signaling.

Associated diseases and disorders

Elevated or diminished levels of IgG are associated with conditions like autoimmune diseases and immunodeficiencies. For example rheumatoid arthritis can involve abnormal IgG response where alterations in Fc glycosylation impact its function connecting IgG to the disorder. In immunodeficiencies such as common variable immunodeficiency (CVID) patients may have low levels of IgG leading to increased susceptibility to infections. IgG in these diseases interacts with proteins like cytokines and immune receptors influencing disease progression.

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