Modeling of EBV Infection and Antibody Responses in Kenyan Infants with Different Levels of Malaria Exposure Shows Maternal Antibody Decay is a Major Determinant of Early EBV Infection

Abstract

The combination of Epstein-Barr virus (EBV) infection and high malaria exposure are risk factors for endemic Burkitt lymphoma, and evidence suggests that infants in regions of high malaria exposure have earlier EBV infection and increased EBV reactivation. Here we analysed the longitudinal antibody response to EBV in Kenyan infants with different levels of malaria exposure. We found that high malaria exposure was associated with a faster decline of maternally-derived IgG antibody to both the EBV viral capsid antigen (VCA) and Epstein-Barr virus nuclear antigen (EBNA1), followed by a more rapid rise in antibody response to EBV antigens in children from the high malaria region. In addition, we observed the long-term persistence of anti-VCA IgM responses in children from the malaria high region. More rapid decay of maternal antibodies was a major predictor of EBV infection outcome, as decay predicted time-to EBV DNA detection, independent of high and low malaria exposure.