TY - JOUR
T1 - Effect of Malaria Infection on Epstein-Barr Virus Persistence in Kenyan Children
AU - Samayoa-Reyes, Gabriela
AU - Weigel, Christoph
AU - Koech, Emmily
AU - Waomba, Kevin
AU - Jackson, Conner
AU - Onditi, Ian A.
AU - Sabourin, Katherine R.
AU - Kenney, Shannon
AU - Baiocchi, Robert A.
AU - Oakes, Christopher C.
AU - Ogolla, Sidney
AU - Rochford, Rosemary
N1 - Publisher Copyright:
© 2023 The Author(s). Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved.
PY - 2024/1/15
Y1 - 2024/1/15
N2 - Background: The 2 cofactors in the etiology of Burkitt lymphoma (BL) are Epstein-Barr virus (EBV) and repeated Plasmodium falciparum malaria infections. This study evaluated EBV loads in mucosal and systemic compartments of children with malaria and controls. Age was analyzed as a covariate because immunity to malaria in endemic regions is age dependent. Methods: Children (2-10 years) with clinical malaria from Western Kenya and community controls without malaria were enrolled. Saliva and blood samples were collected, EBV viral load was assessed by quantitative polymerase chain reaction, and EpiTYPER MassARRAY was used to assess methylation of 3 different EBV genes. Results: Regardless of the compartment, we detected EBV more frequently in malaria cases compared to controls, although the difference was not significant. When EBV was detected, there were no differences in viral load between cases and controls. However, EBV methylation was significantly lower in the malaria group compared to controls in both plasma and saliva (P <. 05), indicating increased EBV lytic replication. In younger children before development of immunity to malaria, there was a significant effect of malaria on EBV load in peripheral blood mononuclear cells (P =. 04). Conclusions: These data suggest that malaria can directly modulate EBV persistence in children, increasing their risk for BL.
AB - Background: The 2 cofactors in the etiology of Burkitt lymphoma (BL) are Epstein-Barr virus (EBV) and repeated Plasmodium falciparum malaria infections. This study evaluated EBV loads in mucosal and systemic compartments of children with malaria and controls. Age was analyzed as a covariate because immunity to malaria in endemic regions is age dependent. Methods: Children (2-10 years) with clinical malaria from Western Kenya and community controls without malaria were enrolled. Saliva and blood samples were collected, EBV viral load was assessed by quantitative polymerase chain reaction, and EpiTYPER MassARRAY was used to assess methylation of 3 different EBV genes. Results: Regardless of the compartment, we detected EBV more frequently in malaria cases compared to controls, although the difference was not significant. When EBV was detected, there were no differences in viral load between cases and controls. However, EBV methylation was significantly lower in the malaria group compared to controls in both plasma and saliva (P <. 05), indicating increased EBV lytic replication. In younger children before development of immunity to malaria, there was a significant effect of malaria on EBV load in peripheral blood mononuclear cells (P =. 04). Conclusions: These data suggest that malaria can directly modulate EBV persistence in children, increasing their risk for BL.
KW - Burkitt lymphoma
KW - EBV methylation
KW - EpiTYPER
KW - Epstein-Barr virus
KW - malaria
UR - http://www.scopus.com/inward/record.url?scp=85170842469&partnerID=8YFLogxK
U2 - 10.1093/infdis/jiad264
DO - 10.1093/infdis/jiad264
M3 - Article
C2 - 37433031
AN - SCOPUS:85170842469
SN - 0022-1899
VL - 229
SP - 73
EP - 82
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 1
ER -