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ASSOCIATION OF FC RECEPTOR IIA (CD32) POLYMORPHISM WITH MALARIAL ANEMIA AND HIGH-DENSITY PARASITEMIA IN INFANTS AND YOUNG CHILDREN

Protective immunity against Plasmodium falciparum is partially mediated through binding of malaria-specific IgG antibodies to Fc receptors. Polymorphic variability in Fc RIIa (H/R-131) is associated with differential binding of IgG subtypes and malaria disease outcomes. However, the role of Fc RIIa-131 variability in conditioning susceptibility to severe malarial anemia, the primary manifestation of severe malaria in holoendemic P. falciparum transmission areas, is largely undefined. Thus, Fc RIIa-H131R polymorphism was investigated in 493 children who came to a hospital with acute malaria. Variation in Fc RIIa-131 was not significantly associated with severe malarial anemia (hemoglobin [Hb] < 6.0 g/dL) or malaria anemia (Hb < 8.0 g/dL). However, relative to the heterozygous genotype, homozygotes for the R131 alleles were protected against high-density parasitemia ( 10,000 parasites/µL; odds ratio [OR] = 0.58, 95% confidence interval [CI] = 0.37–0.92, P = 0.02), while homozygotes for the H131 alleles were mildly protective (OR = 0.71, 95% CI = 0.45–1.13, P = 0.14). Additional multivariate analyses showed that infection with human immunodeficiency virus type 1 did not influence the associations between FcRIIa-H131R polymorphism and malaria disease outcomes. Genotypic results presented here parallel data illustrating that parasite density is unrelated to the severity of anemia in children with acute malaria. Thus, although homozygosity for the R131 allele protects against high-density parasitemia, FcRIIa-131 polymorphism does not protect against malaria anemia.

Received August 12, 2005. Accepted for publication September 27, 2005.

Acknowledgments: We thank the Siaya District Hospital team and the University of Pittsburgh/Kenya Medical Research Institute staff for their technical support. We also thank all the parents and guardians of the study participants and the children who participated in the study. These data are published with the approval of Dr. Davy Koech, Director of Kenya Medical Research Institute.

Financial support: This work was supported by grants from the National Institute of Health (AI51305-02 and TW05884-02) to Douglas J. Perkins.

Disclosure: None of the authors has any conflicts of interest due to commercial or other affiliations.

^* Address correspondence to Douglas J. Perkins, Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, 130 DeSoto Street, 603 Parran Hall, Pittsburgh, PA 15261. E-mail: djp{at}pitt.edu

Authors’ addresses: Collins Ouma, Dorothy A. Opondo, Tom Were, Richard O. Otieno, and John M. Ong’echa, University of Pittsburgh/Kenya Medical Research Institute Laboratories of Parasitic and Viral Diseases, Kisumu, Kenya and Center for Vector Biology and Control Research, Medical Research Institute, P.O. Box 1578, Kisumu, Kenya. Christopher C. Keller and Douglas J. Perkins, Department of Infectious Diseases and Microbiology, University of Pittsburgh, 603 Parran Hall, 130 DeSoto Street, Pittsburgh, PA 15261, PA, Telephone: 412-624-5894, Fax: 412-624-4953, E-mail: djp{at}pitt.edu. Michael F. Otieno, Department of Pre-Clinical Sciences, Kenyatta University, P.O. Box 43844, Nairobi, Kenya. Alloys S. S. Orago, National AIDS Control Council, P.O. Box 61307, Nairobi, Kenya. John M. Vulule, Center for Vector Biology and Control Research, P.O. Box 1578, Kisumu, Kenya. Robert E. Ferrell, Department of Human Genetics, University of Pittsburgh, Graduate School of Public Health, A304 Crabtree Hall, DeSoto Street, Pittsburgh, PA 15261, Telephone: 412-624-3018, Fax: 412-624-3020.

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