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    Human Epstein-Barr virus early antigen diffuse (EBV-EA-D) IgG ELISA Kit

    Regulatory status: For research use only, not for use in diagnostic procedures.

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    Sample
    Serum, plasma
    Species Reactivity
    Human
    Intended Use
    The ELISA test kit provides semiquantitative or quantitative in vitro determination of human antibodies of the immunoglobulin class IgG against Epstein-Barr virus early antigen diffuse (EBV-EA-D) in serum or plasma to support the diagnosis of infectious mononucleosis.
    Contents of Kit
    1. Microplate wells coated with antigens, 12 microplate strips each containing 8 individual break-off wells in a frame, ready for use,12 x 8
    2. Calibrator 1, 200 RU/ml (IgG, human), ready for use, dark red, 1 x 2.0 ml
    3. Calibrator 2, 20 RU/ml (IgG, human), ready for use, red 1 x 2.0 ml
    4. Calibrator 3, 2 RU/ml (IgG, human), ready for use, light red, 1 x 2.0 ml
    5. Positive control, (IgG, human), ready for use, blue 1 x 2.0 ml
    6. Negative control, (IgG, human), ready for use green 1 x 2.0 ml
    7. Enzyme conjugate, peroxidase-labelled anti-human IgG (rabbit), ready for use, green, 1 x 12 ml
    8. Sample buffer, ready for use, light blue, 1 x 100 ml
    9. Wash buffer, 10x concentrate, colourless, 1 x 100 ml
    10. Chromogen/substrate solution, TMB/H2O2, ready for use, colourless, 1 x 12 ml
    11. Stop solution, 0.5 M sulphuric acid, ready for use, colourless, 1 x 12 ml
    12. Test instruction --- 1 booklet
    13. Quality control certificate --- 1 protocol
    Storage
    The test kit has to be stored at a temperature between +2°C and +8°C. Do not freeze. Unopened, all test kit components are stable until the indicated expiry date.
    Performance Characteristics
    Calibration:
    As no international reference serum exists for antibodies against EBV-EA-D, the calibration is performed in relative units (RU). For every group of tests performed, the extinction readings of the calibrators and the relative units and/or ratios determined for the positive and negative controls must lie within the limits stated for the relevant test kit lot. A quality control certificate containing these reference values is included. If the values specified for the controls are not achieved, the test results may be inaccurate and the test should be repeated.
    The binding activity of the antibodies and the activity of the enzyme used is temperature-dependent. It is therefore recommended using a thermostat in all three incubation steps. The higher the room temperature (+18°C to +25°C) during incubation steps, the greater will be the extinction. Corresponding variations apply also to the incubation times. However, the calibrators are subject to the same influences, with the result that such variations will be largelycompensated in the calculation of the result.
    Antigen:
    The microplate wells were coated with the recombinant Epstein-Barr virus early antigen diffuse. The protein was expressed in E. coli and the molecular weight is 45 kDa.
    Detection Limit
    The lower detection limit is defined as the mean value of an analyte-free sample plus three times the standard deviation and is the smallest detectable antibody titer. The lower detection limit of the EBV- EA-D IgG ELISA kit is 0.8 RU/ml.
    Sensitivity
    General Description
    Since early EBV antigens (early antigen, EA) are expressed in the lytic replication phase, the detection of specific antibodies using the Anti-EBV-EA-D IgG ELISA Kit can contribute to supporting the diagnosis of active EBV infections. Results should always be interpreted within the context of clinical symptoms and with respect to further laboratory diagnostic analyses.
    Citations Publication Publication (1)
    Have you cited DEIA329 in a publication? Let us know and earn a reward for your research.
    Lehikoinen, Joonas, et al. "High Epstein-Barr virus capsid antigen IgG level associates with the carriership of CD8+ T cell somatic mutations in the STAT3 SH2 domain." Clinical Immunology 255 (2023): 109733.
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    The Epstein-Barr virus (EBV) early antigen (EA) complex is made up of multiple proteins that can be helpful in diagnosing EBV-related diseases. There are two forms of EA: diffuse and restricted, which are found in different parts of the cell. The diffuse EA is expressed during the early phase of the virus replicating. When someone is infected with EBV for the first time, their immune response typically includes the presence of IgM and IgG antibodies to the viral capsid antigen (VCA) and EA, but no antibodies to the Epstein-Barr nuclear antigen (EBNA-1).

    In immunocompetent adolescents or adults, primary EBV infection often leads to infectious mononucleosis (IM), a usually self-limiting illness. It is characterized by fatigue, fever, sore throat, and swollen lymph nodes. IM is diagnosed based on symptoms and blood tests. EBV is the main cause of IM, but other infections, such as hepatitis A, hepatitis B, or hepatitis C, rubella, and toxoplasmosis can have similar symptoms. Testing helps distinguish between different infections and rules out other causes.

    However, EBV serology can vary widely among individuals, making the diagnosis of IM through serological testing complicated. To overcome this challenge, a combination of EBV serological markers is usually used for detection. Reports suggest that testing for VCA IgM, VCA IgG, and EBNA IgG together is generally sufficient for diagnosing acute, past, or no EBV infection. Patients with primary infections typically have both VCA IgM and VCA IgG antibodies, but no EBNA-1 IgG antibodies. In contrast, past infections are characterized by the presence of VCA IgG and EBNA-1 IgG antibodies, but no VCA IgM antibodies. The presence of EBNA-1 IgG is particularly important because a positive result definitively rules out an acute EBV infection. The diagnostic role of EA IgG is debated, as it can be present in both acute and reactivated infections. However, in the absence of EBNA-1 IgG, a positive EA IgG result suggests acute infection. Combining EA IgG testing with other markers aids in the stage-specific diagnosis of EBV infection.

    Alternative Names

    Human Epstein-Barr virus early antigen diffuse (EBV-EA-D) IgG ELISA
    Human EBV early antigen diffuse IgG ELISA
    Human EBV-EA-D IgG ELISA
    Human EBV early antigen diffuse IgG ELISA Kit
    Human EBV-EA-D IgG ELISA Kit

    Customer Reviews

    Smoking and Epstein-Barr virus infection in multiple sclerosis development

    SCIENTIFIC REPORTS

    Authors: Hedstrom, Anna Karin; Huang, Jesse; Brenner, Nicole; Butt, Julia; Hillert, Jan; Waterboer, Tim; Kockum, Ingrid; Olsson, Tomas; Alfredsson, Lars

    It is unclear whether smoking interacts with different aspects of Epstein-Barr virus (EBV) infection with regard to multiple sclerosis (MS) risk. We aimed to investigate whether smoking acts synergistically with elevated EBNA-1 antibody levels or infectious mononucleosis (IM) history regarding MS risk. Two Swedish population-based case-control studies were used (6,340 cases and 6,219 matched controls). Subjects with different smoking, EBNA-1 and IM status were compared regarding MS risk, by calculating odds ratios (OR) with 95% confidence intervals (CI) employing logistic regression. Potential interaction on the additive scale was evaluated by calculating the attributable proportion due to interaction (AP). Current and past smokers had higher EBNA-1 antibody levels than never smokers (p < 0.0001). There was an additive interaction between current smoking and high EBNA-1 antibody levels (AP 0.3, 95% CI 0.2-0.4), but not between past smoking and high EBNA-1 antibody levels (AP 0.01, 95% CI -0.1 to 0.1), with regard to MS risk. An interaction also occurred between current smoking and IM history (AP 0.2, 95% CI 0.004-0.4), but not between past smoking and IM history (AP -0.06, 95% CI -0.4 to 0.3). Current smoking increases EBNA-1 antibody levels and acts synergistically with both aspects of EBV infection to increase MS risk, indicating that there is at least one pathway to disease in which both risk factors are involved.

    Epstein-Barr virus—recent advances

    The Lancet Infectious Diseases

    Authors: Macsween K F, Crawford D H.

    Epstein–Barr virus is a tumorigenic herpes virus that is ubiquitous in the adult population. The virus is generally spread to and between young children through salivary contact, and only causes clinical illness where primary infection is delayed until adolescence or beyond, when an intense immunopathological reaction leads to the symptoms of infectious mononucleosis in roughly 50% of cases. More than 90% of the world's population carry Epstein–Barr virus as a life-long, latent infection of B lymphocytes. Recent data show that by mimicking B-cell antigen-activation pathways the virus enters the long-lived memory B lymphocyte pool where it evades immune elimination by severely restricting its own gene expression. By influencing B-cell survival mechanisms Epstein–Barr virus may induce tumours such as B lymphoproliferative disease and Hodgkin's disease. Vaccines are being developed to prevent and/or treat these conditions, but an animal model is required to study pathogenesis before a rational vaccine strategy can be formulated.

    Epstein-Barr virus and cancer

    Clinical Cancer Research

    Authors: Thompson M P, Kurzrock R.

    EBV was the first human virus to be directly implicated in carcinogenesis. It infects >90% of the world's population. Although most humans coexist with the virus without serious sequelae, a small proportion will develop tumors. Normal host populations can have vastly different susceptibility to EBV-related tumors as demonstrated by geographical and immunological variations in the prevalence of these cancers. EBV has been implicated in the pathogenesis of Burkitt's lymphoma, Hodgkin's disease, non-Hodgkin's lymphoma, nasopharyngeal carcinoma, and lymphomas, as well as leiomyosarcomas arising in immunocompromised individuals. The presence of this virus has also been associated with epithelial malignancies arising in the gastric region and the breast, although some of this work remains in dispute. EBV uses its viral proteins, the actions of which mimic several growth factors, transcription factors, and antiapoptotic factors, to usurp control of the cellular pathways that regulate diverse homeostatic cellular functions. Recent advances in antiviral therapeutics, application of monoclonal antibodies, and generation of EBV-specific CTLs are beginning to show promise in the treatment of EBV-related disorders.
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