Description

The Diagnostic Automation, Inc. Epstein-Barr Virus-Viral Capsid Antigen (EBV-VCA) IgM ELISA kit, is intended for the detection of IgM antibody to Epstein-Barr virus in human serum.

Purified EBV-VCA antigen is coated on the surface of microwells. Diluted patient serum is added to wells, and the EBV-VCA IgM specific antibody, if present, binds to the antigen. All unbound materials are washed away. After adding enzyme conjugate, it binds to the antibody-antigen complex. Excess enzyme conjugate is washed off, and TMB Chromogenic substrate is added. The enzyme conjugate catalytic reaction is stopped at a specific time. The intensity of the color generated is proportional to the amount of IgG specific antibody in the sample. The results are read by a microwell reader compared in a parallel manner with calibrator and controls.
Purified EBV-VCA antigen is coated on the surface of microwells. Diluted patient serum is added to wells, and the EBV-VCA IgM specific antibody, if present, binds to the antigen. All unbound materials are washed away. After adding enzyme conjugate, it binds to the antibody-antigen complex. Excess enzyme conjugate is washed off, and TMB Chromogenic substrate is added. The enzyme conjugate catalytic reaction is stopped at a specific time. The intensity of the color generated is proportional to the amount of IgG specific antibody in the sample. The results are read by a microwell reader compared in a parallel manner with calibrator and controls.

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 IM.
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. 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-factor.

In the last two decades, serological methods have progressed from testing for the presence of non-specific heterophile antibodies to measuring levels of IgG or IgM formed against subunits of EBV antigen complexes. One of the best indicators of active EBV infection is antibody to viral capsid antigens, structural proteins necessary for replication of the virus.

Viral capsid antigens are present in every cell infected with EBV. The IgM response to VCA is among the earliest detectable humoral immune responses, usually present at the onset of the disease and peaking within four to six weeks. VCA-IgM levels are also transient, declining rapidly and usually becoming undetectable within two to three months from onset of clinical symptoms.