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 Blood, 1 July 2007, Vol. 110, No. 1, pp. 18-28.
Prepublished online as a Blood First Edition Paper on March 6, 2007; DOI 10.1182/blood-2006-09-018069.

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REVIEW IN TRANSLATIONAL HEMATOLOGY

Malarial anemia: of mice and men

Abigail A. Lamikanra1, Douglas Brown2, Alexandre Potocnik2, Climent Casals-Pascual1,3, Jean Langhorne2, and David J. Roberts1

1 Nuffield Department of Clinical Laboratory Sciences and National Blood Service Oxford Centre, John Radcliffe Hospital, Oxford, United Kingdom; 2 National Institute for Medical Research, The Ridgeway, London, United Kingdom; 3 Medical Research Council Laboratory, Atlantic Road, Fajara, Gambia

Severe malaria is manifest by a variety of clinical syndromes dependent on properties of both the host and the parasite. In young infants, severe malarial anemia (SMA) is the most common syndrome of severe disease and contributes substantially to the considerable mortality and morbidity from malaria. There is now growing evidence, from both human and mouse studies of malaria, to show that anemia is due not only to increased hemolysis of infected and clearance of uninfected red blood cells (RBCs) but also to an inability of the infected host to produce an adequate erythroid response. In this review, we will summarize the recent clinical and experimental studies of malaria to highlight similarities and differences in human and mouse pathology that result in anemia and so inform the use of mouse models in the study of severe malarial anemia in humans.


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