The test system provides detection of human antibodies of the immunoglobulin class IgG against Epstein-Barr virus early antigen (EBV-EA).
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 × 8 2. Calibrator 1, 200 RU/ml (IgG, human), ready for use, dark red, 1 × 2.0 ml 3. Calibrator 2, 20 RU/ml (IgG, human), ready for use, red 1 × 2.0 ml 4. Calibrator 3, 2 RU/ml (IgG, human), ready for use, light red, 1 × 2.0 ml 5. Positive control, (IgG, human), ready for use, blue 1 × 2.0 ml 6. Negative control, (IgG, human), ready for use green 1 × 2.0 ml 7. Enzyme conjugate, peroxidase-labelled anti-human IgG (rabbit), ready for use, green, 1 × 12 ml 8. Sample buffer, ready for use, light blue, 1 × 100 ml 9. Wash buffer, 10x concentrate, colourless, 1 × 100 ml 10. Chromogen/substrate solution, TMB/H2O2, ready for use, colourless, 1 × 12 ml 11. Stop solution, 0.5 M sulphuric acid, ready for use, colourless, 1 × 12 ml 12. Test instruction --- 1 booklet 13. Quality control certificate --- 1 protocol
Storage
The product has to be stored at +2 °C to +8 °C; do not freeze! Unopened, the product is stable until the indicated expiry date. Do not use the product after the expiry date.
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.
Standard Curve
Ratio-based The test can be evaluated by calculating a ratio of the extinction value of the control or sample over the extinction value of calibrator 2. Calculate the ratio according to the following formula: Extinction of the control or sample / Extinction of calibrator 2 =Ratio The cut-off recommended is 1.0 ratio. We recommend evaluating results as follows: Not detected: Ratio <0.8 Borderline detected: Ratio ≥0.8 to <1.1 Detected: Ratio ≥1.1 For duplicate determinations the mean of the two values should be taken. 3-point-calibrated The standard curve from which the concentration of antibodies in the samples can be taken is obtained by plotting of the extinction values measured for the 3 calibrators against the corresponding units (linear/line- ar). Use the "point-to-point"evaluation method for the calculation of the standard curve. The following plot is an example of a typical calibration curve. Please do not use this curve for the determination of antibody concentrations in samples. f the extinction for a sample lles above that of calibrator 1 (200 RU/mL). the result should be given as">200 RU/mL". It is recommended that this sample be remeasured in a new test nun at a dilution of e.g 1:404, The result in RU/mL read from the standard curve must then be multiplied by the respective dilution factor. The cut-off recommended is 20 Relative Units. We recommend evaluating results as follows: Not detected: <16 RU/ml Borderline detected: ≥16 to <22 RU/ml Detected: ≥22 RU/ml For duplicate determinations the mean of the two values should be taken.
Citations
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High Epstein-Barr virus capsid antigen IgG level associates with the carriership of CD8+ T cell somatic mutations in the STAT3 SH2 domain
Joonas Lehikoinen, Miko Valori, Anne J Jääskeläinen, Sini M Laakso, T Petteri Arstila, Pentti J Tienari
Applications: ELISA Reactive species: Human
"Abstract: High carrier prevalence of STAT3 SH2 domain somatic mutations was recently discovered in CD8+ T cells. We found these low-allele-fraction clones in 26% of donors, without difference between multiple sclerosis (MS) patients and controls. Here we tested whether anti-viral antibodies associate with the carriership of these mutant clones. We compared antibody responses against common viruses in mutation carriers vs. non-carriers. Plasma samples of 152 donors (92 MS patients, 60 controls) were analyzed for antibodies against cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus-6A and parvovirus B19. The mutation carrier status associated with EBV VCA IgG level (p = 0.005) and remained significant after logistic regression (p = 0.036). This association was contributed similarly by MS patients and controls. These results suggest that EBV contributes to the generation or growth of these clones. The pathogenic role of the STAT3 mutant clones in MS is presently unclear, but their detailed characterization warrants further study." Article snippet: Additionally, we analyzed Human herpesvirus 6A (HHV6A) IgG antibodies with Qualitative Human Herpesvirus 6A Antibody IgG ELISA Kit (*) and EBV early antigen with Human Epstein-Barr virus early antigen diffuse (EA-D) IgG ELISA Kit (Creative Diagnostics®, USA, Cat: DEIA329) according to manufacturer's instructions.
Figure 1. Associations of age, sex, HLA-DR15 and MS diagnosis with virus antibodies (univariate and multivariate p-values)
Background
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
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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.
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.
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.
COA
![The purity of recombinant EBV [His] >95%, determined by SDS-PAGE](https://resource.creative-diagnostics.com/diagnostics/productimages-1/DAG1578-1.jpg)
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Figure 1. Associations of age, sex, HLA-DR15 and MS diagnosis with virus antibodies (univariate and multivariate p-values) 
