Genetic polymorphisms in TLR4, CR1 and Duffy genes are not associated with malaria resistance in patients from Baixo Amazonas region, Brazil.
The main purpose of this research was to analyze the relation of the genetic polymorphisms frequently expressed by antigen-presenting cells, erythrocytes and malaria susceptibility/resistance with the human malaria infection cases. The sample used consisted of 23 Plasmodium vivax (Pv)- and P. falciparum (Pf)-infected patients, and 21 healthy individuals as a control group, from the Baixo Amazonas population in Pará, Brazil. The Asp299Gly polymorphisms in the Toll-like receptor 4 (TLR4), and Gly42Asp, Arg89Cys, Ala100Thr, and T-33C in the Duffy gene (FY) were analyzed by restriction fragment length polymorphism-polymerase chain reaction. The Lys1590Glu and Arg1601Gly polymorphisms in the complement receptor type 1 (CR1) were analyzed by DNA sequencing. According to the results obtained and statistical analysis considering a significance level or alpha = 0.01, we conclude that the low heterozygote frequency (2.27%) for the Asp299Gly mutation, detected in the TLR4 gene, is not related to the Pv and Pf infections in the patients analyzed. Also, the promoter region GATA-1 analysis of the FY gene in the Pv-infected patients showed that the heterozygote frequency for the T-33C mutation (11.36% of the infected patients and 20.45% of the control patients) is not related to infection resistance. Regarding the CR1 gene, the observed heterozygote frequency (9.09%) for the Arg1601Gly mutation in Pf-infected patients when compared to heterozygote frequency in the control group (18.18%) suggests that there is no correlation with infection resistance.
Soares
S C
SC
Departamento de Clínica Médica, Faculdade de Medicina, Universidade de São Paulo, Ribeirão Preto, SP, Brasil. simone@uea.edu.br
Abé-Sandes
K
K
Nascimento Filho
V B
VB
Nunes
F M F
FM
Silva
W A
WA
D000818:Animals; D001938:Brazil / Q000453:epidemiology; D004375:Duffy Blood-Group System / Q000235:genetics*; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D008288:Malaria / Q000453:epidemiology / Q000235:genetics*; D009154:Mutation; D010963:Plasmodium falciparum / Q000472:pathogenicity; D010966:Plasmodium vivax / Q000472:pathogenicity; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011956:Receptors, Cell Surface / Q000235:genetics*; D017463:Receptors, Complement 3b / Q000235:genetics*; D051197:Toll-Like Receptor 4 / Q000235:genetics*
C473745:ACKR1 protein, human; C509991:CR1 protein, human; D004375:Duffy Blood-Group System; D011956:Receptors, Cell Surface; D017463:Receptors, Complement 3b; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4