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目的 了解氯喹单用及与青蒿琥脂伍用治疗恶性疟前后 ,pfcrt和 pfmdr1抗药性有关基因的点突变变化特征。 方法 使用PCR RFLP技术检测基因点突变。 结果 氯喹及与青蒿琥脂伍用治疗前后的所有样本都发现有恶性疟原虫pfcrt基因氨基酸编码 76突变为苏氨酸的特征。但是 ,氯喹治疗前 ,5 0 % pfmdr1基因氨基酸编码 86为天冬酰氨酸 (野生型 ) ,而剩余的 5 0 %为野生型和突变型 (苏氨酸 )的特征。氯喹治疗后 ,在 18个复燃的病例中 ,83 .3 %的 pfmdr1基因 86位点为野生型 ,剩余的 16.7%是混合型。氯喹与青蒿琥脂伍用治疗前 ,3个样本携带混合型基因型 ,剩余的 (86% )为野生型 ,但治疗后 ,所有样本只携带野生型。 结论 这些结果可能支持这样的假说 :pfcrt基因突变起主导作用 ,但 pfmdr1基因突变增强了氯喹抗药性的效果。
Objective To investigate the characteristics of point mutation of pfcrt and pfmdr1 resistance genes in chloroquine alone and before and after treatment with artesunate. Methods PCR RFLP was used to detect point mutations. Results Chloroquine and artesunate with all samples before and after treatment found that the pfcrt gene of Plasmodium falciparum was encoded by amino acid number 76 to threonine. However, 50% of the pfmdr1 gene amino acids encode asparagine (wild type) prior to chloroquine treatment, while the remaining 50% are characterized by both wild-type and mutant (threonine). After chloroquine treatment, 83.3% of the pfmdr1 gene 86 loci were wild type in the 18 relapsed cases, and the remaining 16.7% were mixed. Three samples had mixed genotypes before treatment with chloroquine and artesunate, and the remaining (86%) were wild-type, but all samples carried wild-type after treatment. Conclusions These results may support the hypothesis that mutations in the pfcrt gene predominate but mutations in the pfmdr1 gene enhance the chloroquine resistance.