恶性疟原虫基因组进化主要通过DNA排列如基因重复事件,删除和插入基因转换,易位,(韦伦医生等人。1990;1992年坎普,掀起等人。1997)。单核苷酸多态性主要贡献的差异性。机制在恶性疟原虫抗氯喹(CQ)被调查和抗恶性疟原虫CQ转运体基因的突变(Pfcrt)位于7号染色体多药耐药性恶性疟原虫蛋白1(pfmrp1)位于5号染色体和恶性疟原虫耐多药耐药基因1(pfmdr1)位于5号染色体上,牵连其中。替换赖氨酸苏氨酸的密码子76年K76T pfcrt基因,显示体外与CQ耐药性有关隔离来自亚洲,非洲,南美洲,和巴布亚新几内亚。(Fidock et al .,2000,Djimde et al .,2001)。测序pfcrt编码基因的开放阅读框显示突变氨基酸152年和163年。Substituiton 152和丝氨酸苏氨酸为丙氨酸密码子的精氨酸密码子163 pfcrt基因也被报道与氯喹的数量显著减少累积的寄生虫,尽管他们扮演的角色在对氯喹尚未探索的长度。这个基因的序列多态性在72 – 76位置与地理起源有关寄生虫样本,与CVIET模式在耐药隔离来自亚洲和非洲,和耐SVMNT隔离从巴布亚新几内亚和南美洲。2000年(Fidock et al,Mehlotra et al . 2001年)。耐药基因突变的pfmdr1天冬酰胺酪氨酸在位置86(N86Y)与体外耐药菌株。(福特等人。1990)尽管中国的参与是不清楚,有人建议pfmdr1突变可能会带来一些优势寄生虫的CQ的存在,从而增加CQ阻力水平。
Polymorphisms of the P.falciparum genome have mainly evolved through DNA arrangement such as gene duplication events, gene conversions, translocation, deletions and insertions (Wellens et. al. 1990; Kemp 1992, Deitch et. al. 1997). Single nucleotide polymorphisms contribute largely to the variability. The mechanism of chloroquine (CQ) resistance in Plasmodium falciparum has been investigated and mutations in the P. falciparum CQ resistance transporter gene (Pfcrt) located on chromosome 7, P. falciparum Multidrug Resistance Protein 1 (pfmrp1) located on chromosome 5 and the P. falciparum multidrug resistant gene 1 (pfmdr1) located on chromosome 5, have been implicated. The substitution of threonine for lysine in codon 76, K76T in the pfcrt gene, was shown in vitro to be associated with CQ resistance in isolates from Asia, Africa, South America, and Papua New Guinea.(Fidock et al., 2000, Djimde et al., 2001). Sequencing of the open reading frame of the pfcrt coding gene showed mutations at amino acid 152 and 163. Substituiton of threonine for alanine at codon 152 and serine for arginine at codon 163 in the pfcrt gene have also been reported with significant reduction in the amount of chloroquine accumulated by the parasite though the role they play in resistance to chloroquine has not been explored in length. Sequence polymorphisms at position 72-76 of this gene have been associated with the geographic origin of parasite samples, with the CVIET pattern in resistant isolates from Asia and Africa, and with SVMNT in resistant isolates from Papua New Guinea and South America.( Fidock et al 2000, Mehlotra et al. 2001). The multidrug resistant gene pfmdr1 with a mutation of asparagine to tyrosine at position 86 (N86Y) has been associated with in vitro resistant strains.(Foote et. al. 1990) Although its participation is not clear, it has been suggested that the pfmdr1 mutation may confer some advantage to the parasite in the presence of CQ, thus increasing the level of CQ resistance.