Up to 500 millions are affected by malaria parasite each year and only 1% of them develop severe clinical forms of the disease. No full satisfactory explanation for the fact that only small proportion of malaria infected individuals develops severe clinical phenotypes while others don’t. The aims of the present study is to assess the role of TNF-α - 308 G>A in predisposing to cerebral malaria in children in Central Sudan. 109 children admitted with cerebral malaria (CM) were enrolled in this study (Mean age 6.1± 3.3 years old). The onset of cerebral malaria in the study subjects started in the first two years of life with no gender effect and the highest incidence of the disease was at the age group (4 - 6 years old). The allele frequencies in control group (n= 109) were 0.91 for TNFα-308G (TNF1) and 0.09 for TNFα-308A (TNF2) and the allele frequencies in 93 CM subjects were 0.95 for TNFα-308G (TNF1) and 0.05 for TNFα-308A (TNF2). The distribution of TNFα -308 genotypes in normal group was consistent with the Hardy-Weinberg equilibrium. No TNF2 homozygote was observed among CM subjects. However, the distribution of TNFα-308 genotypes and alleles did not differ significantly between CM patients and controls (P = 0.271). These data suggest that TNF2 is not associated with predisposition to CM in Central Sudanese children. Further studies for confirmation of this finding in other regions of Sudan are required.
Key words: Cerebral malaria, genetic susceptibility, cytokine, TNF.
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