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Malaria has been the greatest scourge of humankind for many millennia, and as a consequence has had more impact than any other pathogen in shaping the human genome. The sequencing of the human genome provides a new opportunity to determine the genetic traits that confer resistance to infection or disease. The identification of these traits can reveal immune responses, or host–parasite interactions, which may be useful for designing vaccines or new drugs. Similarly, the parasite genome sequence is being exploited to accelerate the development of new antimalarial interventions, for example by identifying parasite metabolic pathways that may be targeted by drugs. The malaria parasites are well known for their ability to undergo antigenic variation, and in parallel to cause a diverse array of disease syndromes, including the severe syndromes that commonly cause death. Genome-based technologies are being harnessed to relate gene and protein expression levels, or genetic variation, to the parasite forms that are targets of protective immunity. Well-conducted clinical studies are required to relate host or parasite diversity with disease. However, genomics studies of human populations raise important ethical issues, such as the disposition of data related to disease susceptibility or paternity, and the ability of communities to understand the nature of the research.
Received August 21, 2006. Accepted for publication April 14, 2007.
Acknowledgments: DPK and MD thank their colleagues in the Malaria Genomic Epidemiology Network for collaborations. PED thanks M. Fried for ideas and discussions.
Financial support: FN is a member of the Malaria Immunology and Pathogenesis Network (MIMPAC). DPK receives support from the Medical Research Council, Wellcome Trust, Bill and Melinda Gates Foundation and Grand Challenges in Global Health. MD receives support from the International Atomic Energy Authority and the Bill & Melinda Gates Foundation. PED receives support from Bill & Melinda Gates Foundation (Grant 29202), Grand Challenges in Global Health/ Foundation for NIH (Grant 1364), US Department of Defense (Award W81XWH-05-2-0014), the US National Institutes of Health (R01AI52059 and U19AI065664), and the Fogarty International Center/NIH (D43 TW05509-04).
* Address correspondence to Patrick E. Duffy, Seattle Biomedical Research Institute, 307 Westlake Avenue North, Suite 500, Seattle WA 98109. E-mail: patrick.duffy{at}sbri.org.
Authors addresses: Francine Ntoumi, Hopital Albert Schweitzer, Research Unit, Lambarene B P. Box 118, Gabon, E-mail: ntoumi{at}edctp.org. Dominic Kwiatkowski and Mahamadou Diakité, Wellcome Trust Centre for Human Genetics Roosevelt Drive, Oxford OX3 7BN, and Wellcome Trust Sanger Institute, Hinxton, United Kingdom, E-mail: dominic.kwiatkowski{at}paediatrics.ox.ac.uk. Theonest K. Mutabingwa, MOMS Project, PO Box 476, Morogoro Regional Hospital, Morogoro, Tanzania, E-mail: tmutabingwa{at}sbri.org. Patrick E. Duffy, Seattle Biomedical Research Institute,307 Westlake Avenue North, Suite 500, Seattle WA 98109, E-mail: patrick.duffy{at}sbri.org.
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