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Does apolipoprotein E polymorphism influence susceptibility to malaria?
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  1. M A Wozniak1,
  2. E B Faragher2,
  3. J A Todd3,
  4. K A Koram4,
  5. E M Riley3,
  6. R F Itzhaki1
  1. 1Molecular Neurobiology Laboratory, Department of Optometry and Neuroscience, UMIST, Manchester, UK
  2. 2Manchester School of Management, UMIST, Manchester, UK
  3. 3Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, UK
  4. 4Noguchi Memorial Institute for Medical Research, University of Ghana, Ghana
  1. Correspondence to:
 Professor R F Itzhaki, Molecular Neurobiology Laboratory, Department of Optometry and Neuroscience, UMIST, Manchester M60 1QD, UK; 
 ruth.itzhaki{at}umist.ac.uk

Abstract

Outcome of infection varies greatly among people, and in the case of three very different viruses, it is determined by apolipoprotein E (APOE) genotype. APOE might affect outcome of malaria infection also, since apoE protein and the protozoon (like the viruses) share cell entry mediators (heparan sulphate proteoglycans and/or specific apoE receptors). APOE polymorphisms give rise to protein variants that differ in binding strength to these mediators; thus, the extent of competition between apoE and protozoon for cell entry, and hence magnitude of protozoan damage, might depend on apoE isoform. Genotypes of infants infected with malaria were examined. It was found that APOE ε2 homozygotes became infected at an earlier age than those carrying the other genotypes, the difference being statistically significant. Parasite densities, all of which were low, did not differ significantly. This effect, although based on small numbers, suggests that APOE ε2 may be a risk factor for early infection.

  • malaria
  • apolipoprotein E
  • gene-infectious agent interactions
  • susceptibility

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