Description

The Diagnostic Automation, Inc. Epstein Barr Virus Early Antigen (EBV-EA) IgG ELISA kit, is intended for the detection of IgG antibody to Epstein Barr Virus Nuclear Antigen-1 in human sera and plasma.

Purified EBV-EA antigen is coated on the surface of microwells. Diluted patient serum is added to wells, the anti- EBV-EA specific antibody, if present, will bind 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 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 its characteristic morphology.

EBV infection may demonstrate a wide spectrum of clinical symptoms. The majority of primary EBV infections is transmitted via saliva, occurs during childhood, and is subclinical. Antibody titers to specific EBV antigens correlate with different stages of IM. Both IgM and IgG antibodies to the viral capsid antigen (VCA) peak 3 to 4 weeks after primary EBV infection. IgM anti-VCA declines rapidly and is usually undetectable after 12 weeks. IgG anti-VCA titers decline slowly after peaking but last indefinitely. Antibodies to EBV nuclear antigen (EBNA) detected by anticomplement immunofluorescence develop from 1 month to 6 months after infection; and, like anti-VCA, persist indefinitely. Antibodies to EBNA indicate that the EBV infection was not recent. EBV early antigen (EA) consists of two components; diffuse (D), and restricted (R). The terms D and R reflect the different patterns of immunofluorescence staining exhibited by the two components. Antibodies to EA may appear transiently for up to three months or longer during the acute phase of IM in 85% of patients7. The antibody response to EA in IM patients is usually to the D component, whereas silent seroconversion to EBV in children may produce antibodies to the R components. A definitive diagnosis of primary EBV infection can be made with 95% of acute phase sera based on antibody titers to VCA, EBNA, and EA.

Antibodies to EA, usually to the R component, together with antibodies to EBNA and high titers of IgG anti- VCA, may be associated with reactivation of the latent viral carrier state. EBV positive serology associated with reactivation of EBV is found in sera of patients with immunodeficiencies8, patients with recurrent parotitis immunosuppressed patients, pregnant women, and persons of advanced age. Antibodies to the R component may be found at moderate to high levels in patients with Burkitt�s lymphoma. In contrast, patients with nasopharyngeal carcinoma may produce high titer antibodies to the D component. Elevated levels of anti-EA and IgG anti-VCA may be detected in patients with chronic or recurrent illness suspected of being caused by EBV. However, a diagnosis of chronic EBV should not be based on the presence of antibodies to EA since elevated anti-EA titers may also be found in patients with other diseases as well as in healthy individuals with past EBV infections.