Background: Infectious mononucleosis is the common clinical manifestation of primary Epstein-Barr virus (EBV) infection in young children. We evaluated a chemiluminescent immunoassay method for the determination of serum anti-viral capsid antigen IgM antibody and its clinical value in the diagnosis of infectious mononucleosis. Methods: Concentrations of the antibody in serum samples from 187 children measured by chemiluminescent immunoassay were compared with those measured by ELISA. Results: Assessment of technologic quality (methodology) in diagnostic tests demonstrated that sensitivity of CLIA was 0.64 U/ ml and the functional sensitivity was < 0.9 U/ml. The within-assay and the between-assay imprecisions of different concentrations were all < 5%. Recoveries were all in 93-107%. The linear regression equation between expected values and measured values was y=0.0967+1.0093x, correlation coefficient was 0.9996 (p < 0.0001). The ROC curve showed that the sensitivity and specificity of the CLIA both were > 90%. The area under the curve was 0.992, which was significantly higher than that of ELISA (p < 0.05). Conclusion: The CLIA was the excellent method for EBV-VCA IgM measurement at present and can improve the clinical diagnosis of infectious mononucleosis. (c) 2004 Elsevier B.V. All rights reserved.

Epstein-Barr virus (EBV) is a necessary cause of endemic Burkitt lymphoma (eBL), while the role of Plasmodium falciparum in eBL remains uncertain. This study aimed to generate new hypotheses on the interplay between both infections in the development of eBL by investigating the IgG and IgM profiles against several EBV and P. falciparum antigens. Serum samples collected in a childhood study in Malawi (2005-2006) from 442 HIV-seronegative children (271 eBL cases and 171 controls) between 1.4 and 15 years old were tested by quantitative suspension array technology against a newly developed multiplex panel combining 4 EBV antigens [Z Epstein-Barr replication activator protein (ZEBRA), early antigen-diffuse component (EA-D), EBV nuclear antigen 1, and viral capsid antigen p18 subunit (VCA-p18)] and 15 P. falciparum antigens selected for their immunogenicity, role in malaria pathogenesis, and presence in different parasite stages. Principal component analyses, multivariate logistic models, and elastic-net regressions were used. As expected, elevated levels of EBV IgG (especially against the lytic antigens ZEBRA, EA-D, and VCA-p18) were strongly associated with eBL [high vs low tertile odds ratio (OR) = 8.67, 95% confidence interval (CI) = 4.81-15.64]. Higher IgG responses to the merozoite surface protein 3 were observed in children with eBL compared with controls (OR = 1.29, 95% CI = 1.02-1.64), showing an additive interaction with EBV IgGs (OR = 10.6, 95% CI = 5.1-22.2, P = 0.05). Using elastic-net regression models, eBL serological profile was further characterized by lower IgM levels against P. falciparum preerythrocytic-stage antigen CelTOS and EBV lytic antigen VCA-p18 compared with controls. In a secondary analysis, abdominal Burkitt lymphoma had lower IgM to EBV and higher IgG to EA-D levels than cases with head involvement. Overall, this exploratory study confirmed the strong role of EBV in eBL and identified differential IgG and IgM patterns to erythrocytic vs preerythrocytic P. falciparum antigens that suggest a more persistent/chronic malaria exposure and a weaker IgM immune response in children with eBL compared with controls. Future studies should continue exploring how the malaria infection status and the immune response to P. falciparum interact with EBV infection in the development of eBL.