EBV Conference 2008 Guangzhou - Baylor College of Medicine

50 (RegID: 1252)
R. Njie
Institution: Cancer Research UK Institute for Cancer Studies, School of Cancer Sciences, The University
of Birmingham, Birmingham, UK.
E-mail:
THE EFFECTS OF ACUTE MALARIA ON EBV LOAD AND EBV-SPECIFIC T CELL
IMMUNITY IN GAMBIAN CHILDREN
R. Njie, A. Bell, H. Jia, D. Croom-Carter, S. Chaganti, A. Hislop, H. Whittle and A. Rickinson
Oralabstract:
Endemic Burkitt lymphoma (BL) is the commonest cancer of childhood in equatorial areas of Africa and
is consistently EBV genome–positive. In addition to EBV, epidemiologic evidence also strongly
implicates high exposure to Plasmodium Falciparum malaria as a second risk factor for developing
endemic BL. However it is unclear whether malarial infection might pre-dispose the host to endemic BL
through acting as a chronic stimulus to the B cell system and/or through a suppression of EBV-specific T
cell surveillance. In this study, we have analysed the effect of acute malaria on the EBV-host balance using
Q-PCR assays to determine virus genome load in peripheral blood mononuclear cells and
interferon-gamma Elispot assays to enumerate virus-specific CD8+ T cells. We found that Gambian
children, sampled during an acute malaria attack and again up to 6 weeks later, sustained extremely high
virus loads, reaching levels similar to those seen in infectious mononucleosis patients in the UK. Gambian
controls (children and adults with no recent history of malaria) had lower viral loads, though these were
still >10-fold above the median for healthy UK adults. Limited studies with EBV epitope peptides
(restricted through the HLA-B*3501 and -B*5301 alleles) also suggested an impairment of virus-specific
CD8+ T cell function in malarial children, but only during acute disease. The results indicate that acute
malaria is associated with a sustained increase in EBV load and, possibly, a transient decrease in
EBV-specific T cell surveillance. However, whether these two phenomena, increased EBV load and T cell
impairment, are causally linked remains to be resolved. We infer that the unusually high EBV loads in P.
falciparum-challenged populations, allied to the parasite’s capacity to act as a chronic B cell stimulus, are
likely contributory factors in endemic BL pathogenesis.
EBV Conference 2008 Guangzhou
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