Evaluation Of Epstein Barr Viral Load And Antibodies In Children Living In The Malaria Holoendemic Lake Victoria Basin

ABSTRACT

Epstein Barr virus (EBV) and P. falciparum malaria have an overlapping distribution and are incriminated as the primary causal agents for endemic Burkitt‘s lymphoma. Nevertheless, the exact mechanism utilized by these two pathogens to cause endemic Burkitt‘s lymphoma has remained elusive. This study therefore sought to provide insights as to whether presence of Epstein Barr Virus in children who develop severe malaria reveals unique serological/nucleic acid signatures that would allow future development of predictive markers for evolution of Burkitt‘s lymphoma. In this study we determined the viral loads as well as the serological signatures to various Epstein Barr virus antigens in children with complicated and uncomplicated malaria. Children with severe malarial anemia were age and sex matched to those with uncomplicated malaria. Epstein Barr virus -DNA viral load was quantified by real time quantitative PCR and viral load extrapolated from a standard graph using an Epstein Barr virus sample of known copy numbers. IgG and IgM antibody levels to viral capsid antigen and Epstein Barr virus nuclear antigen were determined by enzyme linked immuno-assay. B-cell numbers that are the target for Epstein Barr virus was enumerated by flow cytometery. Of the 94 subjects analyzed, 53% (N=25 in each arm) had detectable EBV load. The geometric mean viral copy number/mL was higher in children with severe malaria (27,556± 25,377 SE) compared to those with mild malaria (21,703±17,434 SE). The mean B-cell numbers were higher in cases (2307+ 551 SE) than controls (1273+ 426 SE). The mean viral capsid antigen IgG titers were significantly higher in the cases (0.97± 0.05 SE) compared to controls (0.79± 0.06 SE ± P0.04). There was no difference in the titers of the other antibodies analyzed. Findings of this study are consistent with early childhood exposure to Epstein Barr virus. The higher viral load and viral capsid antigen IgG antibody in children with severe malaria is attributed to the expansion of infected B-lymphocytes, probably fueled by malaria antigenic stimuli.