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Genetic determinants of anti-malarial acquired immunity in a large multi-centre study. 2015
Jennifer M G Shelton, and
Patrick Corran, and
Paul Risley, and
Nilupa Silva, and
Christina Hubbart, and
Anna Jeffreys, and
Kate Rowlands, and
Rachel Craik, and
Victoria Cornelius, and
Meike Hensmann, and
Sile Molloy, and
Nuno Sepulveda, and
Taane G Clark, and
Gavin Band, and
Geraldine M Clarke, and
Christopher C A Spencer, and
Angeliki Kerasidou, and
Susana Campino, and
Sarah Auburn, and
Adama Tall, and
Alioune Badara Ly, and
Odile Mercereau-Puijalon, and
Anavaj Sakuntabhai, and
Abdoulaye Djimdé, and
Boubacar Maiga, and
Ousmane Touré, and
Ogobara K Doumbo, and
Amagana Dolo, and
Marita Troye-Blomberg, and
Valentina D Mangano, and
Frederica Verra, and
David Modiano, and
Edith Bougouma, and
Sodiomon B Sirima, and
Muntaser Ibrahim, and
Ayman Hussain, and
Nahid Eid, and
Abier Elzein, and
Hiba Mohammed, and
Ahmed Elhassan, and
Ibrahim Elhassan, and
Thomas N Williams, and
Carolyne Ndila, and
Alexander Macharia, and
Kevin Marsh, and
Alphaxard Manjurano, and
Hugh Reyburn, and
Martha Lemnge, and
Deus Ishengoma, and
Richard Carter, and
Nadira Karunaweera, and
Deepika Fernando, and
Rajika Dewasurendra, and
Christopher J Drakeley, and
Eleanor M Riley, and
Dominic P Kwiatkowski, and
Kirk A Rockett, and
Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, UK. jennifer.shelton@well.ox.ac.uk.
BACKGROUND Many studies report associations between human genetic factors and immunity to malaria but few have been reliably replicated. These studies are usually country-specific, use small sample sizes and are not directly comparable due to differences in methodologies. This study brings together samples and data collected from multiple sites across Africa and Asia to use standardized methods to look for consistent genetic effects on anti-malarial antibody levels. METHODS Sera, DNA samples and clinical data were collected from 13,299 individuals from ten sites in Senegal, Mali, Burkina Faso, Sudan, Kenya, Tanzania, and Sri Lanka using standardized methods. DNA was extracted and typed for 202 Single Nucleotide Polymorphisms with known associations to malaria or antibody production, and antibody levels to four clinical grade malarial antigens [AMA1, MSP1, MSP2, and (NANP)4] plus total IgE were measured by ELISA techniques. Regression models were used to investigate the associations of clinical and genetic factors with antibody levels. RESULTS Malaria infection increased levels of antibodies to malaria antigens and, as expected, stable predictors of anti-malarial antibody levels included age, seasonality, location, and ethnicity. Correlations between antibodies to blood-stage antigens AMA1, MSP1 and MSP2 were higher between themselves than with antibodies to the (NANP)4 epitope of the pre-erythrocytic circumsporozoite protein, while there was little or no correlation with total IgE levels. Individuals with sickle cell trait had significantly lower antibody levels to all blood-stage antigens, and recessive homozygotes for CD36 (rs321198) had significantly lower anti-malarial antibody levels to MSP2. CONCLUSIONS Although the most significant finding with a consistent effect across sites was for sickle cell trait, its effect is likely to be via reducing a microscopically positive parasitaemia rather than directly on antibody levels. However, this study does demonstrate a framework for the feasibility of combining data from sites with heterogeneous malaria transmission levels across Africa and Asia with which to explore genetic effects on anti-malarial immunity.
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Victoria Cornelius, and
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