Association of cd36 + 188 T/G gene polymorphism with outcome of cerebral malaria among Sudanese children

Abstract Background Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, which is a major cause of morbidity and mortality, particularly among children in endemic regions. The sequestration of parasitized red blood cells (PRBCs) in the microvasculature of the brain is a critical pathogenic event in CM. The CD36 protein, expressed on endothelial cells, plays a key role in this sequestration. This study aimed to investigate the association of the CD36 + 188 T/G gene polymorphism with the outcome of Cerebral Malaria among a cohort of Sudanese children. Methods One Hundred children were diagnosed with CM and selected for the cohort study. Genomic DNA was extracted and the CD36 + 188 T/G gene polymorphism was genotyped using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Clinical and laboratory data were collected to assess the severity and outcome of the disease. Results The cases fatality rate associated study subjects was 11% ( n = 11) where, 89% ( n = 89) were discharged alive, of them, 7.9% ( n = 7) survived with neurological sequelae. Assessment of effect of the mutant allele in the disease outcome, A statistically significant difference in the distribution of CD36 + 188 T/G genotypes was observed across cerebral malaria outcome groups ( P = 0.046). Further assessment of association of the polymorphisms with mortality, revealed that children carrying the mutant G allele, either in the heterozygous (T/G) or homozygous mutant (G/G) state, were at significantly increased risk of poor outcomes, including death or survival with neurological sequelae. Under the dominant model of inheritance, which best fitted the data, children carrying at least one G allele were approximately eight times more likely to die from cerebral malaria compared with those homozygous for the normal allele (OR = 7.98; 95% CI: 2.09–30.56; P = 0.002). Conclusion The findings suggest that the CD36 + 188 T/G gene polymorphism may play a significant role in influencing the clinical outcome of Cerebral Malaria among Sudanese children. Further research is warranted to fully understand the mechanistic link between this genetic variation and disease pathogenesis.