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
Authors
Reynaldi, ArnoldSchlub, Timothy E.
Piriou, Erwan
Ogolla, Sidney
Sumba, Odada P.
Moormann, Ann M.
Rochford, Rosemary
Davenport, Miles P.
UMass Chan Affiliations
Program in Molecular MedicineDocument Type
Journal ArticlePublication Date
2016-11-01Keywords
Burkitt LymphomaEpstein-Barr virus
P. falciparum malaria
antibody
immunity
Immunology and Infectious Disease
Infectious Disease
Parasitic Diseases
Metadata
Show full item recordAbstract
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. In this study we analyzed 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 immunoglobulin G antibody to both the EBV viral capsid antigen and EBV nuclear antigen, followed by a more rapid rise in antibody response to EBV antigens in children from the high-malaria-transmission region. We also observed the long-term persistence of anti-viral capsid antigen immunoglobulin M responses in children from the high-malaria region. More rapid decay of maternal antibodies was a major predictor of EBV infection outcome, because decay predicted time to EBV DNA detection, independent of high or low malaria exposure.Source
J Infect Dis. 2016 Nov 1;214(9):1390-1398. Epub 2016 Aug 28. Link to article on publisher's siteDOI
10.1093/infdis/jiw396Permanent Link to this Item
http://hdl.handle.net/20.500.14038/29091PubMed ID
27571902Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1093/infdis/jiw396