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EBV VCA IgA ELISA Kit

EBV VCA IgA Reactivity: Epstein-Barr Virus (EBV) Colorimetric Competition ELISA Serum
Catalog No. ABIN996986
  • Target
    EBV VCA IgA (Anti-Epstein-Barr Virus Viral Capsid Antigen IgA (EBV VCA IgA))
    Reactivity
    Epstein-Barr Virus (EBV)
    Detection Method
    Colorimetric
    Method Type
    Competition ELISA
    Application
    ELISA
    Purpose
    Epstein-Barr Virus-Viral Capsid Antigen (EBV-VCA) IgA Enzyme-linked Immunosorbent Assay (ELISA), is intended for the detection of IgA antibody to Epstein-Barr virus in human sera and plasma
    Sample Type
    Serum
    Analytical Method
    Qualitative
    Specificity
    100%
    Sensitivity
    100%
  • Sample Volume
    5 μL
    Assay Time
    1 - 2 h
    Plate
    Pre-coated
    Restrictions
    For Research Use only
  • Storage
    4 °C
    Expiry Date
    12-18 months
  • Target
    EBV VCA IgA (Anti-Epstein-Barr Virus Viral Capsid Antigen IgA (EBV VCA IgA))
    Alternative Name
    Epstein Barr Virus VCA IgA (EBV, VCA IgA)
    Target Type
    Antibody, Antibody
    Background
    Detection of the Epstein-Barr virus was first described in 1964 by Epstein, Achong, and Barr using electron microscopic studies of cultured lymphoblasts derived from patients with Burkitt’s lymphoma. EBV is classified as a member of the herpes-virus family based upon it’s characteristic morphology. EBV infection may demonstrate a wide spectrum of clinical symptoms. The majority of primary EBV infections are transmitted via saliva, occur during childhood, and are subclinical. In the U.S., 50% of the population demonstrate EBV antibodies before the age of 5 years, 80% by adulthood. Transfusion-associated EBV infections have also been reported. In young adults, EBV infection may be clinically manifested as Infectious Mononucleosis (IM) with typical symptoms of sore throat, fever, and lymphadenopathy. College students and military personnel are often cited as a high morbidity incidence population for IM3. Following primary EBV infection, it is postulated that the B lymphocyte may continue to harbor the EBV genome and establish a latent infection that may extend through life. Reactivation of EBV infection or enhanced EBV activation has been documented in immunodeficient or immunosuppressed patients, i.e., organ transplant patients, individuals with malignancies, pregnant women, and persons of advanced age.

    Epstein-Barr virus has also been associated in the pathogenesis of two human cancers, Burkitt’s lymphoma and nasopharyngeal carcinoma (NCP). Documentation by means of DNA hybridization studies demonstrates the presence of the EBV genome on biopsy specimens taken from individuals with these carcinomas. Burkitt’s lymphoma is primarily observed in Sub-Sahara Africa, especially in African children, and in New Guinea. Malarial infections are usually diagnosed in Burkitt’s lymphoma patients and are suggested to be a co-factor. Nasopharyngeal carcinoma is observed in Asia, most notably in Southern China, and may have genetic or environmental influences as the co-factor5,6. Serological studies have shown that the clinical onset of NPC is preceded by the appearance of a high antibody titer of IgA to viral capsid antigens and early antigens. The titers increase with the total tumor burden and the antibodies decline with the response to therapy. In patients with confirmed clinical remission elevation of IgA serological titers is highly significant for prediction of relapse.
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