title: 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. 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.
authors: Infection Analytics Program, Kirby Institute for Infection and Immunity, UNSW Australia, Sydney.
authors: Arnold
authors: A
authors: Reynaldi
authors: Sydney School of Public Health, Sydney University, New South Wales, Australia.
authors: Timothy E
authors: TE
authors: Schlub
authors: Médecins Sans Frontières, Amsterdam, The Netherlands.
authors: Erwan
authors: E
authors: Piriou
authors: Centre for Global Health Research, Kenya Medical Research Institute, Kisumu.
authors: Sidney
authors: S
authors: Ogolla
authors: Centre for Global Health Research, Kenya Medical Research Institute, Kisumu.
authors: Odada P
authors: OP
authors: Sumba
authors: Program in Molecular Medicine, University of Massachusetts Medical School, Worcester.
authors: Ann M
authors: AM
authors: Moormann
authors: Department of Immunology and Microbiology, University of Colorado Denver, Aurora.
authors: Rosemary
authors: R
authors: Rochford
authors: Infection Analytics Program, Kirby Institute for Infection and Immunity, UNSW Australia, Sydney.
authors: Miles P
authors: MP
authors: Davenport
mesh_terms: D000914:Antibodies, Viral / Q000276:immunology*; D000917:Antibody Formation / Q000276:immunology*; D000956:Antigens, Viral / Q000276:immunology; D002051:Burkitt Lymphoma / Q000209:etiology / Q000276:immunology; D036022:Capsid Proteins / Q000276:immunology; D020031:Epstein-Barr Virus Infections / Q000209:etiology* / Q000276:immunology*; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D007223:Infant; D007231:Infant, Newborn; D007630:Kenya; D008288:Malaria / Q000150:complications* / Q000276:immunology*; D019562:Viral Load / Q000276:immunology
chemical_list: D000914:Antibodies, Viral; D000956:Antigens, Viral; D036022:Capsid Proteins; C041788:Epstein-Barr viral capsid antigen; D007074:Immunoglobulin G; D007075:Immunoglobulin M
keywords: Burkitt Lymphoma; Epstein-Barr virus; P. falciparum malaria; antibody; immunity