EBV Glycoprotein 125 (DAG3085)

Product Overview
EBV gp125 Concentrate
Predominantly a single band in non-reducingSDS-PAGE
Approximately 120 μg/mL
2-8°C short term, -20°C long term
The Epstein–Barrvirus (EBV), also called human herpesvirus 4 (HHV-4), is a virus of theherpes family, which includes herpes simplex virus 1 and 2, and is one of themost common viruses in humans. It is best known as the cause of infectiousmononucleosis. It is also associated with particular forms of cancer, particularlyHodgkin"s lymphoma, Burkitt"s lymphoma, nasopharyngeal carcinoma, and centralnervous system lymphomas associated with HIV. Finally, there is evidence thatinfection with the virus is associated with a higher risk of certainautoimmune diseases, especially dermatomyositis, systemic lupuserythematosus, rheumatoid arthritis and multiplesclerosis.
Antigen Description
Glycoproteins are proteins that contain oligosaccharide chains (glycans) covalently attached to polypeptide side-chains. The carbohydrate is attached to the protein in a cotranslational or posttranslational modification. This process is known as glycosyla
EBV gp125 Antigen; Epstein Barr Virus, Viral Capsid Antigen, gp 125; EBV gp125; gp125; EBV; Epstein Barr virus; EpsteinBarr virus viral capsid antigen; HHV4; Human Herpesvirus 4; Major capsidprotein; MCP; Herpesviridae; Gammaherpesvirinae; Lymphocryptovir


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Serodiagnosis of Epstein-Barr virus infection by using recombinant viral capsid antigen fragments and autologous gene fusion


Authors: Hinderer, W; Lang, D; Rothe, M; Vornhagen, R; Sonneborn, HH; Wolf, H

Using recombinant 15- to 30-kDa fragments and fusion with glutathione S-transferase (GST), we investigated the seroreactivity of three large structural proteins of Epstein-Barr virus (EBV), p150 (BcLF1, capsid), p143 (BNRF1, tegument), and gp125 (BALF4, membrane) in Western blots. None of 13 fragments tested, however, was qualified for diagnostic application. In contrast, the two small viral capsid antigens (VCA), p18 (BFRF3) and p23 (BLRF2), demonstrated sensitive (100%) EBV-specific immunoglobulin G (IgG) reactivities, While p18 additionally showed maximum sensitivity for IgM detection, the IgM sensitivity of p23 was restricted (44%), An autologous fusion protein, p23-p18, which consists N-terminally of full-length p23, followed by the carboxy half of p18, was constructed. This antigen was subjected to indirect VCA enzyme-linked immunosorbent assays (ELISAs), for IgG and IgM, as well as to a mu-capture (mu c) IgM ELISA. All assays were found to be 100% specific when EBV-negative sera were tested. Using sera from previously infected individuals, the p23-p18 fusion revealed an improved IgG sensitivity of 99% compared to sensitivities of 97 and 93% for the single antigens p18 and p23, respectively. The sensitivity and specificity of the indirect IgM ELISA with samples of primary and past infections, respectively, were 100%, The pc principle for IgM overcame completely the interference by rheumatoid factors. Compared to the specificity of the indirect IgM version, the specificity with sera collected from rheumatoid arthritis patients increased from 48 to 100%, In summary, the p23-p18 IgG and mu c IgM ELISAs showed excellent performances and are promising new diagnostic tests for the detection of EBV-specific antiviral capsid antibodies.

Henoch-Schonlein purpura associated with primary active Epstein-Barr virus infection: a case report


Authors: Karakayali, Burcu; Yilmaz, Sila; Cakir, Deniz; Gunes, Pembe Gul; Guven, Sirin; Islek, Ismail

Henoch-Schonlein purpura (HSP) is the most common form of childhood vasculitis. Various viral and bacterial infections, drugs, vaccines, food allergy and even insect bites have been considered as triggering factors in pathogenesis of HSP. Epstein-Barr virus (EBV) infection, which is associated with HSP, have been rarely reported. Herein we present HSP patient possibly caused by EBV infection. A 8-year old boy was admitted to our department with fever, rashes on legs and arms and intermittent mild abdominal pain. Multiple purpuric rashes were on his extremities, abdomen and buttock. Laboratory investigations revealed that monospot test was positive, EBV serology tests; Anti-EA-D Ig G: 3+, Anti-VCA gp125 Ig G: 3+, Anti-VCA p19 Ig M: 2+, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig G: negative. The patient was interpreted as the primary active acute EBV infection. A skin biopsy showed leucocytoclastic vasculitis. The other viral and bacterial investigations were negative. The patient was diagnosed as HSP vasculitis according to EULAR criteria and treated with intravenous hydration and ibuprofen. He was discharged after 15 days with normal laboratory findings and physical examination. We think that EBV infection may be stimulant factor for autoimmune reactions and may cause HSP vasculitis. Hence, it may be useful to investigate the EBV infection in etiology of HSP cases.

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