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Bio-Rad offers complete microplate EIA kits for the detection of specific IgM and IgG antibodies to Epstein-Barr virus (EBV) antigens, aiding in determination of the stage of the EBV infection.
Bio-Rad offers a comprehensive menu of EIA serology tests using standardized procedure and common reagents.
Epstein-Barr virus (EBV; Human herpesvirus-4) is a human gammaherpesvirus that establishes lifelong infection in B lymphocytes with a predilection for latent, rather than lytic, infection. Epstein-Barr virus is associated with a variety of clinical disorders arising from different pathogenic mechanisms (reviewed in 82).
The syndrome of mononucleosis with atypical lymphocytosis can also be seen during primary infection with several other viruses including human cytomegalovirus, HIV, and Human Herpesvirus 6 (HHV-6), with CMV being the most common.
Individuals with a rare, inherited X-linked immunodeficiency known as X-linked lymphoproliferative syndrome or Duncan's syndrome, are at risk for overwhelming lethal primary infection with Epstein-Barr virus (10, 114).
The presence of IgM antibodies to viral capsid antigen (VCA) is the most sensitive and specific indicator of acute infection (Table 1). The issue of whether nucleoside analogues might be effective during primary gammaherpesvirus infection, where viral replication is more likely to play an important pathogenic role, has been extensively studied in infectious mononucleosis. Unless the history suggests the possibility of other infections such as HIV, a battery of viral serologies is not routinely necessary. As convalescence proceeds, Epstein-Barr nuclear antigen (EBNA) antibodies become detectable and VCA IgM disappears.
Persistent EBV infection is controlled by a virus-specific immune response and is asymptomatic in most humans. Instead, latently infected cell lines are used in which cells can be induced for lytic viral replication in the presence or absence of potential antiviral agents. In 6 different studies involving a total of approximately 320 patients, oral or intravenous acyclovir therapy consistently reduced or eliminated lytic EBV infection during therapy as detected by virus shedding in oropharyngeal secretions but had no effect on clinical outcome, duration of symptoms, or establishment of persistent infection in the oropharynx or peripheral blood B lymphocytes (3, 4, 104, 153, 154, 161). An Epstein-Barr virus deletion mutant associated with fatal lymphoproliferative disease unresponsive to therapy with virus-specific CTLs. Add on new test orders from previously run samples, create custom EBV panels, and interface bidirectionally with the laboratory information system (LIS). After adsorption to the cell surface receptor and virion entry, several Epstein-Barr nuclear antigens (EBNAs) and latent membrane proteins are expressed (1). Definitive diagnosis requires endoscopic biopsy and demonstration of EBV antigen or Epstein-Barr virus-encoded RNA (EBER) expression in malignant tissue. If the presentation is atypical but suggestive of infectious mononucleosis, and the Monospot is negative, EBV serology can confirm the diagnosis or indicate whether testing for other pathogens such as CMV, toxoplasmosis may be appropriate, based on the clinical presentation and history. Antiviral activity is measured by quantifying viral DNA and is expressed as the concentration of drug required to inhibit 50% of viral DNA replication induced by lytic infection (IC50). A prospective clinical study of Epstein-Barr virus and host interactions during acute infectious mononucleosis.
Epstein-Barr virus LMP1 inhibits the expression of SAP gene and upregulates Th1 cytokines in the pathogenesis of hemophagocytic syndrome. Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States. Replication of Epstein-Barr virus DNA in lymphoblastoid cells treated for extended periods with acyclovir.

Effect of acyclovir [9-(2-hydroxyethoxymethyl)guanine] on Epstein- Barr virus DNA replication.
A cohort study among university students: identification of risk factors for Epstein-Barr virus seroconversion and infectious mononucleosis. Successful treatment with ganciclovir of presumed Epstein-Barr meningo-encephalitis following bone marrow transplant. A prospective evaluation of heterophile and Epstein-Barr virus-specific IgM antibody tests in clinical and subclinical infectious mononucleosis: Specificity and sensitivity of the tests and persistence of antibody.
Induction of the Epstein-Barr virus thymidine kinase gene with concomitant nucleoside antivirals as a therapeutic strategy for Epstein- Barr virus-associated malignancies. Adenoviral gene transfer into dendritic cells efficiently amplifies the immune response to LMP2A antigen: a potential treatment strategy for Epstein-Barr virus--positive Hodgkin's lymphoma.
Management of Epstein-Barr virus-induced post-transplant lymphoproliferative disease in recipients of solid organ transplantation. First EBV vaccine trial in humans using recombinant vaccinia virus expressing the major membrane antigen. Determination of risk factors for Epstein-Barr virus-associated posttransplant lymphoproliferative disorder in pediatric liver transplant recipients using objective case ascertainment. Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus infection. Epstein-Barr virus (EBV) induced polyclonal and monoclonal B-cell lymphoproliferative diseases occurring after renal transplantation. Epstein-Barr Virus-Induced B-Cell Lymphoma After Renal Transplantation: Acyclovir Therapy and Transition From Polyclonal to Monoclonal B-Cell Proliferation.
Polymorphism of the interleukin-10 gene is associated with susceptibility to Epstein-Barr virus infection. Long-term serological follow-up of patients for Epstein-Barr virus after recovery from infectious mononucleosis. Epstein-barr virus-associated malignancies: epidemiologic patterns and etiologic implications. Chronic active Epstein-Barr virus infection associated with mutations in perforin that impair its maturation. CD20 monoclonal antibody (rituximab) for therapy of Epstein-Barr virus lymphoma after hemopoietic stem-cell transplantation. XMEN disease: a new primary immunodeficiency affecting Mg2+ regulation of immunity against Epstein-Barr virus.
Prolonged inhibitory effect of 9-(1,3-dihydroxy-2- propoxymethyl)guanine against replication of Epstein-Barr virus. Plasma Epstein-Barr viral load predicting response after chemotherapy for post-transplant lymphoproliferative disease. The Epstein-Barr virus (EBV)-encoded protein kinase, EBV-PK, but not the thymidine kinase (EBV-TK), is required for ganciclovir and acyclovir inhibition of lytic viral production. Selective lack of antibody to a component of EB nuclear antigen in patients with chronic active Epstein-Barr virus infection.
All serology tests are available in 96-test kits, designed for rapid turnaround and manual or automated use.

Currently, treatment of EBV-associated diseases is more often directed against virus-induced tumors or disease symptoms and less frequently against viral replication. Most cases of EBV infection are transmitted by the presence of virus in oropharyngeal secretions of asymptomatic shedders. The higher incidence in this demographic group most likely reflects a later age of primary infection as well as greater access to health care and availability of specific diagnostic tests. Endoscopic brushing with measurement of EBV DNA load and specific EBV mRNAs expressed in tumors may allow less invasive diagnostic testing and follow-up (136). Therefore, IgG VCA antibodies are not usually useful for establishing the presence of active EBV infection since virtually all patients are IgG positive by the time they seek medical attention. Uncontrolled lytic infection in the oropharynx is manifested as oral hairy leukoplakia in immunosuppressed hosts (38) but manifestations of virtually all other lymphoproliferative and malignant diseases associated with EBV are due to latently infected cells. Encephalitis and cerebellitis may be the initial presentation of EBV infection, particularly in children, and may occur despite a negative Monospot test.
Testing for the presence of IgM VCA antibodies and the absence of antibodies to Epstein-Barr nuclear antigen (EBNA) is useful for identifying active and recent infections. One study evaluated the clinical utility of detecting EBV viremia with real-time PCR in children with primary EBV infection compared to controls (108). Both drugs require initial phosphorylation by a viral kinase to be subsequently incorporated into DNA and terminate viral DNA replication. Acyclovir may have some marginal utility in some situations in highly immunocompromised hosts by preventing ongoing production of infectious virions and infection of additional B cells, thereby leading to expansion of the reservoir of infected cells. These results are not surprising since latent infection has already been established and the vigorous host immune response to virus infection responsible for the majority of symptoms has been triggered. The differences observed between infants and young adults with regard to primary infection may relate to the size of the viral inoculum at the time of infection or to the intensity of cellular immune responses driven by EBV-infected B cells. Because antibodies to Epstein-Barr nuclear antigens do not develop until approximately 4 weeks after onset of symptoms and persist for life (49), seroconversion to anti-EBNA positivity is therefore indicative of recent EBV infection. Within the primary infection group, those with detectable virus were more likely to have lymphadenopathy, higher atypical lymphocytes counts, and higher aminotransferases than those without detectable virus.
It has also been shown that in a patient with IM, the virus load decreased as the symptoms resolved (71). Delineation of the cell signaling pathways used by EBV latent genes, such as the tumor necrosis factor receptor pathway by LMP1 (96), may provide unique opportunities to block virus induced cell proliferation or to induce apoptosis of virus infected cells.
Generally speaking, however, EBV viral load testing in peripheral blood provides little information over serology in the immunocompetent patient being neither sensitive nor specific as a test for primary infection. In vitro, only a small fraction of infected cells reactivates lytic infection to produce infectious virions.
In latently EBV-infected cells, the virus exists as a circular DNA molecule, or episome, in the nucleus, and viral DNA is replicated in unison with cell DNA and cell doubling.
In addition, after primary EBV infection, virus may be intermittently shed in the saliva for life (3).

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