IFNGR1 Gene Promoter Polymorphisms and Susceptibility to Cerebral Malaria

Interferon (IFN)-γ is a critical mediator of immunity to malaria. This study explored the relationship between polymorphisms in the promoter region of the gene encoding IFN-γ receptor 1 (IFNGR1) and susceptibility to malaria in African children. Four polymorphisms were found in the region between 21...

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Bibliographic Details
Published in:The Journal of infectious diseases 2002-06, Vol.185 (11), p.1684-1687
Main Authors: Koch, Oliver, Awomoyi, Agnes, Usen, Stanley, Jallow, Muminatou, Richardson, Anna, Hull, Jeremy, Pinder, Margaret, Newport, Melanie, Kwiatkowski, Dominic
Format: Article
Language:English
Subjects:
Adult
Alleles
Biological and medical sciences
Blood
Case-Control Studies
Cerebral malaria
Child
Child, Preschool
Concise Comunications
Ethnic groups
Family
Female
Gambia
Gene Expression Regulation
Genetic Predisposition to Disease - genetics
Genotypes
Haplotypes
Human protozoal diseases
Humans
Infections
Infectious diseases
Interferon gamma Receptor
Malaria
Malaria, Cerebral - genetics
Male
Medical sciences
Mutation
Parasitic diseases
Polymorphism, Genetic - genetics
Promoter Regions, Genetic - genetics
Protozoal diseases
Receptors
Receptors, Interferon - genetics
Receptors, Interferon - metabolism
Sequence Analysis, DNA
Tropical medicine
Umbilical cord
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Summary:Interferon (IFN)-γ is a critical mediator of immunity to malaria. This study explored the relationship between polymorphisms in the promoter region of the gene encoding IFN-γ receptor 1 (IFNGR1) and susceptibility to malaria in African children. Four polymorphisms were found in the region between 21400 and +100 nt of the translational start site by sequencing, and analysis of 562 nuclear families revealed 6 haplotypes. Case-control analysis of 562 Gambian children with severe malaria and 569 umbilical cord blood samples (controls) showed that in Mandinka, the major Gambian ethnic group, heterozygotes for the IFNGR1−56 polymorphism were protected against cerebral malaria (odds ratio, 0.54; P = .016) and against death resulting from cerebral malaria (odds ratio, 0.22; P = .006). Analysis of a family study by transmission disequilibrium testing revealed a similar result. Further data are needed to validate this finding, but these results are reminiscent of those for other well-established heterozygote advantages, such as that associated with hemoglobin S.
ISSN:0022-1899
1537-6613
DOI:10.1086/340516