No evidence for association of the CD40, CD40L and BLYS polymorphisms, B-cell co-stimulatory molecules, with Brazilian endemic Plasmodium vivax malaria

作者：Capobianco Marcela P^*; Cassiano Gustavo C; Furini Adriana A C; Storti Melo Luciane M; Pavarino Erika C; Galbiatti Ana L S; Fraga Valeria D; Conceicao Luciana M; Couto Vanja S C; Couto Alvaro A R A; Machado Ricardo L D

来源：Transactions of the Royal Society of Tropical Medicine and Hygiene, 2013, 107(6): 377-383.

DOI：10.1093/trstmh/trt031

• Malaria
• Plasmodium vivax
• Single nucleotide polymorphism
• CD40L
• CD40
• BLYS

Plasmodium vivax is the most prevalent malaria species in Brazil. The parasite-host coevolutionary process can be viewed as an arms race, in which adaptive genetic changes in one are eventually matched by alterations in the other.
Following the candidate gene approach we analyzed the CD40, CD40L and BLYS genes that participate in B-cell co-stimulation, for associations with P. vivax malaria. The study sample included 97 patients and 103 controls. We extracted DNA using the extraction and purification commercial kit and identified the following SNPs: 1C T in the CD40 gene, 726T C in the CD40L gene and the 871C T in the BLyS gene using PCR-RFLP. We analyzed the genotype and allele frequencies by direct counting. We also compared the observed with the expected genotype frequencies using the Hardy-Weinberg equilibrium.
The allele and genotype frequencies for these SNPs did not differ statistically between patient and control groups. Gene-gene interactions were not observed between the CD40 and BLYS and between the CD40L and BLYS genes. Overall, the genes were in Hardy-Weinberg equilibrium. Significant differences were not observed among the frequencies of antibody responses against P. vivax sporozoite and erythrocytic antigens and the CD40 and BLYS genotypes.
The results of this study show that, although the investigated CD40, CD40L and BLYS alleles differ functionally, this variation does not alter the functionality of the molecules in a way that would interfere in susceptibility to the disease. The variants of these genes may influence the clinical course rather than simply increase or decrease susceptibility.

• 出版日期2013-6