非恶性疟人体疟原虫药物抗性分子标记研究进展
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摘要
随着抗疟药的长期、广泛使用,疟原虫对抗疟药逐渐产生抗性。目前有关恶性疟原虫的抗药性分子标记研究较多,而对非恶性疟原虫关注度相对较小。为了更好地为临床治疗的合理用药提供科学依据,为非恶性疟人体疟原虫对抗疟药敏感性分子监测提供参考,本文就非恶性疟人体疟原虫常见抗药性相关分子标记的研究进展作一综述。
With the long.term and widespread application of antimalarial drugs,Plasmodium falciparum has gradually pro.duced resistance to antimalarial drugs. At present,there are more researches on the molecular markers of P. falciparum drug re.sistance,while less attention has been paid to the molecular markers of non.P. falciparum drug resistance. In order to provide the reference for rational drug use in clinical treatment and reference for molecular monitoring of antimalarial drug sensitivity of non.P. falciparum,this paper reviews the researches on the common molecular markers related to non.P. falciparum drug resistance.
With the long.term and widespread application of antimalarial drugs,Plasmodium falciparum has gradually pro.duced resistance to antimalarial drugs. At present,there are more researches on the molecular markers of P. falciparum drug re.sistance,while less attention has been paid to the molecular markers of non.P. falciparum drug resistance. In order to provide the reference for rational drug use in clinical treatment and reference for molecular monitoring of antimalarial drug sensitivity of non.P. falciparum,this paper reviews the researches on the common molecular markers related to non.P. falciparum drug resistance.
引文
[1] World Health Organization. World malaria report 2017[R]. Geneva:World Health Organization,2018:1-7.
[2] Li PP,Zhao ZJ,Xing H,et al. Plasmodium malariae and Plasmodium ovale infections in the China-Myanmar border area[J]. Malar J,2016,15:557.
[3]徐超,黄炳成,魏庆宽,等.恶性疟原虫与耐药性相关分子遗传标记的研究进展[J].中国病原生物学杂志,2016,11(12):1149-1152.
[4] Ravikumar B,Duden R,Rubinsztein DC. Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy[J]. Hum Mol Genet,2002,11(9):1107-1117.
[5] Ding WX,Yin XM. Mitophagy:mechanisms,pathophysiological roles,and analysis[J]. Biol Chem,2012,393(7):547-564.
[6] Mita T,Tanabe K,Kita K. Spread and evolution of Plasmodium falciparum drug resistance[J]. Parasitol Int,2009,58(3):201-209.
[7] Meunier B,Robert A. Heme as trigger and target for trioxane-containing antimalarial drugs[J]. Acc Chem Res,2010,43(11):1444-1451.
[8] Wang J,Zhang CJ,Chia WN,et al. Haem-activated promiscuous targeting of artemisinin in Plasmodium falciparum[J]. Nat Commun,2015,6:10111.
[9] Eastman RT,Khine P,Huang R,et al. PfCRT and PfMDR1 modulate interactions of artemisinin derivatives and ion channel blockers[J]. Sci Rep,2016,6:25379.
[10] Yuan J,Cheng KC,Johnson RL,et al. Chemical genomic profiling for antimalarial therapies,response signatures,and molecular targets[J]. Science,2011,333(643):724-729.
[11] Lisewski AM,Quiros JP,Ng CL,et al. Supergenomic network compression and the discovery of EXP1 as a glutathione transferase inhibited by artesunate[J]. Cell,2014,158(4):916-928.
[12] Pulcini S,Staines HM,Pittman JK,et al. Expression in yeast links field polymorphisms in PfATP6 to in vitro artemisinin resistance and identifies new inhibitor classes[J]. J Infect Dis,2013,208(3):468-478.
[13] Zhou YQ,Li WC,Xiao YL. Profiling of multiple targets of artemisinin activated by hemin in cancer cell proteome[J]. ACS Chem Biol,2016,11(4):882-888.
[14] WHO. Guidelines for the treatment of malaria[R]. Geneva:World Health Organization. 2006:27-30.
[15] Cooper RA,Lane KD,Deng BB,et al. Mutations in transmembrane domains 1,4 and 9 of the Plasmodium falciparum chloroquine resistance transporter alter susceptibility to chloroquine,quinine and quinidine[J]. Mol Microbiol,2007,63(1):270-282.
[16] Lakshmanan V,Patrick GB,Dominik VP,et al. A critical role for PfCRT K76T in Plasmodium falciparum verapamil-reversible chloroquine resistance[J]. EMBO J,2005,24(13):2294-2305.
[17] Nomura T,Carlton JM,Baird JK,et al. Evidence for different mechanisms of chloroquine resistance in 2 Plasmodium species that cause human malaria[J]. J Infect Dis,2001,183(11):1653-1661.
[18] Fernandez BC,Pinazo MJ,Gonzalez A,et al. Increased expression levels of the pvcrt-o and pvmdr1 genes in a patient with severe Plasmodium vivax malaria[J]. Malar J,2009,8(55):3523-3530.
[19] Melo GC,Wm M,Siqueira AM,et al. Expression levels of pvcrt-o and pvmdr-1 are associated with chloroquine resistance and severe Plasmodium vivax malaria in patients ofthe Brazilian Amazon[J].PLoS One,2014,9(8):e105922.
[20] Pava Z,Handayuni I,Wirjanata G,et al. Expression of Plasmodium vivax crt-o is related to parasite stage but not Ex vivo chloroquine susceptibility[J]. Antimicrob Agents Chemother,2016,60(1):361-367.
[21] Suwanarusk R,Russell B,Chavchich M,et al. Chloroquine resistant Plasmodium vivax:in vitro characterisation and association with molecular polymorphisms[J]. PLoS One,2007,2(10):e1089.
[22] Golassa L,Erko B,Baliraine FN,et al. Polymorphisms in chloroquine resistance-associated genes in Plasmodium vivax in Ethiopia[J]. Malar J,2015,14:164.
[23] Nyunt MH,Han JH,Wang B,et al. Clinical and molecular surveillance of drug resistant vivax malaria in Myanmar(2009-2016)[J]. Malar J,2017,16(1):117.
[24] Fatih FA,Staines HM,Siner A,et al. Susceptibility of human Plasmodium knowlesi infections to anti-malarials[J]. Malar J,2013,12:425.
[25] Cowman AF,Morry MJ,Biggs BA,et al. Amino acid changes linked to pyrimethamine.resistance in the dihydrofolate reductasethymidylate synthase gene of Plasmodium falciparum[J]. ProcNatl Acad Sci USA,1988,85(23):9109-9113.
[26] Plowe CV,Cortese JF,Djimde A,et al. Mutations in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase and epidemiologic patterns of pyrimethamine-sulfadoxine use and resistance[J]. J Infect Dis,1997,176(6):1590-1596.
[27] Triglia T,Menting JG,Wilson C,et al. Mutations in dihydropteroate synthase are responsible for sulfone and sulfonamide resistance in Plasmodium falciparum[J]. ProcNatl Acad Sci USA,1997,94(25):13944-13949.
[28] De Beer TA,Louw AI,Joubert F. Elucidation of sulfadoxine resistance with structural models of the bifunctional Plasmodium falciparum dihydropterin pyrophosphokinase-dihydropteroate synthase[J]. Bioorg Med Chem,2006,14(13):4433-4443.
[29] Eldin DP,Philippe T,Rachida O,et al. Sequence variations in the Plasmodium vivax dihydrofolate reductase-thymidylate synthase gene and their relationship with pyrimethamine resistance[J]. Mol Biochem Parasitol,1998,92(2):265-273.
[30] Lee WJ,Kim HH,Choi YK,et al. Analysis of the dihydrofolate reductase-thymidylate synthase gene sequences in Plasmodium vivax field isolates that failed chloroquine treatment[J]. Malar J,2010,9:331.
[31] Imwong M,Pukrittakayamee S,Looareesuwan S,et al. Association of genetic mutations in Plasmodium vivax dhfr with resistance to sulfadoxine-pyrimethamine:geographical and clinical correlates[J]. Antimicrob Agents Chemother,2001,45(11):3122-3127.
[32] Marfurt J,De Monbrison F,Brega SA,et al. Molecular markers of in vivo Plasmodium vivax resistance to amodiaquine plus sulfadoxine-pyrimethamine:Mutations in pvdhfr and pvmdr1[J]. J of Infect Dis,2008,198(3):409-417.
[33] Lu F,Lim CS,Nam DH,et al. Mutations in the antifolate-resistance-associated genes dihydrofolate reductase and dihydropteroate synthase in Plasmodium vivax isolates from malaria-endemic countries[J]. Am J Trop Med Hyg,2010,83(3):474-479.
[34] Miao M,Yang Z,Cui L,et al. Different allele prevalence in the dihydrofolate reductase and dihydropteroate synthase genes in Plasmodium vivax populations from China[J]. Am J Trop Med Hyg,2010,83(6):1206-1211.
[35] Zaman J,Shahbazi A,Asgharzadeh M. Plasmodium vivax dhfr mutations among isolates from malarious areas of Iran[J]. Korean J Parasitol,2011,49(2):125-131.
[36] Thongdee P,Kuesap J,Rungsihirunrat KA,et al. Genetic polymorphisms in Plasmodium vivax dihydrofolate reductase and dihydropteroate synthase in isolates from the Philippines,Bangladesh,and Nepal[J]. Korean J Parasitol,2015,53(2):227-232.
[37] Saralamba N,Nakeesathit S,Mayxay M,et al. Geographic distribution of amino acid mutations in DHFR and DHPS in Plasmodium vivax isolates from Lao PDR,India and Colombia[J]. Malar J,2016,15(1):484.
[38] Sastu UR,Abdullah NR,Norahmad NA,et al. Mutations of pvdhfr and pvdhps genes in vivax endemic-malaria areas in Kota Marudu and Kalabakan,Sabah[J]. Malar J,2016,15:63.
[39] Nyunt MH,Shein T,Zaw NN,et al. Molecular evidence of drug resistance in asymptomatic malaria infections,Myanmar,2015[J]. Emerg Infect Dis,2017,23(3):517-520.
[40] Sutherland CJ. Persistent parasitism:the adaptive biology of malariae and ovale malaria[J]. Trends Parasitol,2016,32(10):808-819.
[41] Tanomsing N,Imwong M,Pukrittayakamee S,et al. Genetic analysis of the dihydrofolate reductase-thymidylate synthase gene from geographically diverse isolates of Plasmodium malariae[J]. Am J Trop Med Hyg,2007,51(10):3523-3530.
[42] Khim N,Kim S,Bouchier C,et al. Reduced impact of pyrimethamine drug pressure on Plasmodium malariae dihydrofolate reductase gene[J]. Antimicrob Agents Chemother,2012,56(2):863-868.
[43] Sutherland CJ,Tanomsing N,Nolder D,et al. Two nonrecombining sympatric forms of the human malaria parasite Plasmodium ovale occur globally[J]. J Infect Dis,2010,201(10):1544-1550.
[44] Tirakarn S,Riangrungroj P,Kongsaeree P,et al. Cloning and heterologous expression of Plasmodium ovale dihydrofolate reductasethymidylate synthase gene[J]. Parasitol Int,2012,61(2):324-332.
[45] Grigg MJ,Barber BE,Marfurt J,et al. Dihydrofolate-reductase mutations in Plasmodium knowlesi appear unrelated to selective drug pressure from putative human-to-human transmission in Sabah,Malaysia[J]. PLoS One,2016,11(3):e0149519.
[46] Ariey F,Witkowski B,Amaratunga CA,et al. A molecular marker of artemisinin-resistant Plasmodium falciparum malaria[J]. Nature,2014,505(7481):50-55.
[47] Popovici J,Kao S,Eal L,et al. Reduced polymorphism in the kelch propeller domain in Plasmodium vivax isolates from Cambodia[J]. Antimicrob Agents Chemother,2015,59(1):730-733.
[48] Talundzic E,Chenet SM,Goldman IF,et al. Genetic analysis and species specific amplification of the artemisinin resistance-associated kelch propeller domain in P. falciparum and P. vivax[J]. PLoS One,2015,10(8):e0136099.
[49] Deng S,Ruan Y,Bai Y,et al. Genetic diversity of the Pvk12 gene in Plasmodium vivax from the China-Myanmar border area[J]. Malar J,2016,15(1):528.
[50] Wang ML,Siddiqui FA,Fan Q,et al. Limited genetic diversity in the PvK12 Kelch protein in Plasmodium vivax isolates from Southeast Asia[J]. Malar J,2016,15(1):537.
[51] Brazeau NF,Hathaway N,Parobek CM,et al. Longitudinal pooled deep sequencing of the Plasmodium vivax K12 kelch gene in Cambodia reveals a lack of selection by artemisinn[J]. Am J Trop Med Hyg,2016,95(6):1409-1412.
[52] Nakeesathit S,Saralamba N,Pukrittayakamee S,et al. Limited polymorphism of the kelch propeller domain in Plasmodium malariae and P. ovale isolates from Thailand[J]. Antimicrob Agents Chemother,2016,60(7):4055-4062.
[53] Sanchez CP,Dave A,Stein WD,et al. Transporters as mediators of drug resistance in Plasmodium falciparum[J]. Int J Parasitol,2010,40(10 SI):1109-1118.
[54] Brega S,Meslin B,De Monbrison F,et al. Identification of the Plasmodium vivax mdr-like gene(pvmdr1)and analysis of singlenucleotide polymorphisms among isolates from different areas of endemicity[J]. J Infect Dis,2005,191(2):272-277.
[55] Rungsihirunrat K,Muhamad P,Chaijaroenkul W,et al. Plasmodium vivax drug resistance genes;pvmdr1 and pvcrt-o polymorphisms in relation to chloroquine sensitivity from a malaria endemic area of Thailand[J]. Korean J Parasitol,2015,53(1):43-49.
[56] Orjuela-Sanchez P,De Santana Filho FS,Chehuan YF,et al.Analysis of single-nucleotide polymorphisms in the crt-o and mdr1genes of Plasmodium vivax among chloroquine-resistant isolates from the Brazilian Amazon region[J]. Antimicrob Agents Chemother,2009,53(8):3561-3564.
[57] Musset L,Bouchaud O,Matheron S,et al. Clinical atovaquoneproguanil resistance of Plasmodium falciparum associated with cytochrome b codon 268 mutations[J]. Microb Infect,2006,8(11):2599-2604.
[58] Barton V,Fisher N,Biagini GA,et al. Inhibiting Plasmodium cytochrome bc1:a complex issue[J]. Curr Opin Chem Biol,2010,14(4):440-446.
[59] Siregar JE,Kurisu G,Kobayashi T,et al. Direct evidence for the atovaquone action on the Plasmodium cytochrome bc1 complex[J].Parasitol Int,2015,64(3):295-300.
[60] Sutherland CJ,Laundy M,Price N,et al. Mutations in the Plasmodium falciparum cytochrome b gene are associated with delayedparasite recrudescence in malaria patients treated with atovaquone-proguanil[J]. Malar J,2008,7:240.
[61]张玲玲,姚立农,陈华良,等.输入性卵形疟原虫细胞色素b,细胞色素c氧化酶Ⅰ和乳酸脱氢酶基因单核苷酸多态性分析[J].中国寄生虫学与寄生虫病杂志,2017,35(5):429-433.
[2] Li PP,Zhao ZJ,Xing H,et al. Plasmodium malariae and Plasmodium ovale infections in the China-Myanmar border area[J]. Malar J,2016,15:557.
[3]徐超,黄炳成,魏庆宽,等.恶性疟原虫与耐药性相关分子遗传标记的研究进展[J].中国病原生物学杂志,2016,11(12):1149-1152.
[4] Ravikumar B,Duden R,Rubinsztein DC. Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy[J]. Hum Mol Genet,2002,11(9):1107-1117.
[5] Ding WX,Yin XM. Mitophagy:mechanisms,pathophysiological roles,and analysis[J]. Biol Chem,2012,393(7):547-564.
[6] Mita T,Tanabe K,Kita K. Spread and evolution of Plasmodium falciparum drug resistance[J]. Parasitol Int,2009,58(3):201-209.
[7] Meunier B,Robert A. Heme as trigger and target for trioxane-containing antimalarial drugs[J]. Acc Chem Res,2010,43(11):1444-1451.
[8] Wang J,Zhang CJ,Chia WN,et al. Haem-activated promiscuous targeting of artemisinin in Plasmodium falciparum[J]. Nat Commun,2015,6:10111.
[9] Eastman RT,Khine P,Huang R,et al. PfCRT and PfMDR1 modulate interactions of artemisinin derivatives and ion channel blockers[J]. Sci Rep,2016,6:25379.
[10] Yuan J,Cheng KC,Johnson RL,et al. Chemical genomic profiling for antimalarial therapies,response signatures,and molecular targets[J]. Science,2011,333(643):724-729.
[11] Lisewski AM,Quiros JP,Ng CL,et al. Supergenomic network compression and the discovery of EXP1 as a glutathione transferase inhibited by artesunate[J]. Cell,2014,158(4):916-928.
[12] Pulcini S,Staines HM,Pittman JK,et al. Expression in yeast links field polymorphisms in PfATP6 to in vitro artemisinin resistance and identifies new inhibitor classes[J]. J Infect Dis,2013,208(3):468-478.
[13] Zhou YQ,Li WC,Xiao YL. Profiling of multiple targets of artemisinin activated by hemin in cancer cell proteome[J]. ACS Chem Biol,2016,11(4):882-888.
[14] WHO. Guidelines for the treatment of malaria[R]. Geneva:World Health Organization. 2006:27-30.
[15] Cooper RA,Lane KD,Deng BB,et al. Mutations in transmembrane domains 1,4 and 9 of the Plasmodium falciparum chloroquine resistance transporter alter susceptibility to chloroquine,quinine and quinidine[J]. Mol Microbiol,2007,63(1):270-282.
[16] Lakshmanan V,Patrick GB,Dominik VP,et al. A critical role for PfCRT K76T in Plasmodium falciparum verapamil-reversible chloroquine resistance[J]. EMBO J,2005,24(13):2294-2305.
[17] Nomura T,Carlton JM,Baird JK,et al. Evidence for different mechanisms of chloroquine resistance in 2 Plasmodium species that cause human malaria[J]. J Infect Dis,2001,183(11):1653-1661.
[18] Fernandez BC,Pinazo MJ,Gonzalez A,et al. Increased expression levels of the pvcrt-o and pvmdr1 genes in a patient with severe Plasmodium vivax malaria[J]. Malar J,2009,8(55):3523-3530.
[19] Melo GC,Wm M,Siqueira AM,et al. Expression levels of pvcrt-o and pvmdr-1 are associated with chloroquine resistance and severe Plasmodium vivax malaria in patients ofthe Brazilian Amazon[J].PLoS One,2014,9(8):e105922.
[20] Pava Z,Handayuni I,Wirjanata G,et al. Expression of Plasmodium vivax crt-o is related to parasite stage but not Ex vivo chloroquine susceptibility[J]. Antimicrob Agents Chemother,2016,60(1):361-367.
[21] Suwanarusk R,Russell B,Chavchich M,et al. Chloroquine resistant Plasmodium vivax:in vitro characterisation and association with molecular polymorphisms[J]. PLoS One,2007,2(10):e1089.
[22] Golassa L,Erko B,Baliraine FN,et al. Polymorphisms in chloroquine resistance-associated genes in Plasmodium vivax in Ethiopia[J]. Malar J,2015,14:164.
[23] Nyunt MH,Han JH,Wang B,et al. Clinical and molecular surveillance of drug resistant vivax malaria in Myanmar(2009-2016)[J]. Malar J,2017,16(1):117.
[24] Fatih FA,Staines HM,Siner A,et al. Susceptibility of human Plasmodium knowlesi infections to anti-malarials[J]. Malar J,2013,12:425.
[25] Cowman AF,Morry MJ,Biggs BA,et al. Amino acid changes linked to pyrimethamine.resistance in the dihydrofolate reductasethymidylate synthase gene of Plasmodium falciparum[J]. ProcNatl Acad Sci USA,1988,85(23):9109-9113.
[26] Plowe CV,Cortese JF,Djimde A,et al. Mutations in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase and epidemiologic patterns of pyrimethamine-sulfadoxine use and resistance[J]. J Infect Dis,1997,176(6):1590-1596.
[27] Triglia T,Menting JG,Wilson C,et al. Mutations in dihydropteroate synthase are responsible for sulfone and sulfonamide resistance in Plasmodium falciparum[J]. ProcNatl Acad Sci USA,1997,94(25):13944-13949.
[28] De Beer TA,Louw AI,Joubert F. Elucidation of sulfadoxine resistance with structural models of the bifunctional Plasmodium falciparum dihydropterin pyrophosphokinase-dihydropteroate synthase[J]. Bioorg Med Chem,2006,14(13):4433-4443.
[29] Eldin DP,Philippe T,Rachida O,et al. Sequence variations in the Plasmodium vivax dihydrofolate reductase-thymidylate synthase gene and their relationship with pyrimethamine resistance[J]. Mol Biochem Parasitol,1998,92(2):265-273.
[30] Lee WJ,Kim HH,Choi YK,et al. Analysis of the dihydrofolate reductase-thymidylate synthase gene sequences in Plasmodium vivax field isolates that failed chloroquine treatment[J]. Malar J,2010,9:331.
[31] Imwong M,Pukrittakayamee S,Looareesuwan S,et al. Association of genetic mutations in Plasmodium vivax dhfr with resistance to sulfadoxine-pyrimethamine:geographical and clinical correlates[J]. Antimicrob Agents Chemother,2001,45(11):3122-3127.
[32] Marfurt J,De Monbrison F,Brega SA,et al. Molecular markers of in vivo Plasmodium vivax resistance to amodiaquine plus sulfadoxine-pyrimethamine:Mutations in pvdhfr and pvmdr1[J]. J of Infect Dis,2008,198(3):409-417.
[33] Lu F,Lim CS,Nam DH,et al. Mutations in the antifolate-resistance-associated genes dihydrofolate reductase and dihydropteroate synthase in Plasmodium vivax isolates from malaria-endemic countries[J]. Am J Trop Med Hyg,2010,83(3):474-479.
[34] Miao M,Yang Z,Cui L,et al. Different allele prevalence in the dihydrofolate reductase and dihydropteroate synthase genes in Plasmodium vivax populations from China[J]. Am J Trop Med Hyg,2010,83(6):1206-1211.
[35] Zaman J,Shahbazi A,Asgharzadeh M. Plasmodium vivax dhfr mutations among isolates from malarious areas of Iran[J]. Korean J Parasitol,2011,49(2):125-131.
[36] Thongdee P,Kuesap J,Rungsihirunrat KA,et al. Genetic polymorphisms in Plasmodium vivax dihydrofolate reductase and dihydropteroate synthase in isolates from the Philippines,Bangladesh,and Nepal[J]. Korean J Parasitol,2015,53(2):227-232.
[37] Saralamba N,Nakeesathit S,Mayxay M,et al. Geographic distribution of amino acid mutations in DHFR and DHPS in Plasmodium vivax isolates from Lao PDR,India and Colombia[J]. Malar J,2016,15(1):484.
[38] Sastu UR,Abdullah NR,Norahmad NA,et al. Mutations of pvdhfr and pvdhps genes in vivax endemic-malaria areas in Kota Marudu and Kalabakan,Sabah[J]. Malar J,2016,15:63.
[39] Nyunt MH,Shein T,Zaw NN,et al. Molecular evidence of drug resistance in asymptomatic malaria infections,Myanmar,2015[J]. Emerg Infect Dis,2017,23(3):517-520.
[40] Sutherland CJ. Persistent parasitism:the adaptive biology of malariae and ovale malaria[J]. Trends Parasitol,2016,32(10):808-819.
[41] Tanomsing N,Imwong M,Pukrittayakamee S,et al. Genetic analysis of the dihydrofolate reductase-thymidylate synthase gene from geographically diverse isolates of Plasmodium malariae[J]. Am J Trop Med Hyg,2007,51(10):3523-3530.
[42] Khim N,Kim S,Bouchier C,et al. Reduced impact of pyrimethamine drug pressure on Plasmodium malariae dihydrofolate reductase gene[J]. Antimicrob Agents Chemother,2012,56(2):863-868.
[43] Sutherland CJ,Tanomsing N,Nolder D,et al. Two nonrecombining sympatric forms of the human malaria parasite Plasmodium ovale occur globally[J]. J Infect Dis,2010,201(10):1544-1550.
[44] Tirakarn S,Riangrungroj P,Kongsaeree P,et al. Cloning and heterologous expression of Plasmodium ovale dihydrofolate reductasethymidylate synthase gene[J]. Parasitol Int,2012,61(2):324-332.
[45] Grigg MJ,Barber BE,Marfurt J,et al. Dihydrofolate-reductase mutations in Plasmodium knowlesi appear unrelated to selective drug pressure from putative human-to-human transmission in Sabah,Malaysia[J]. PLoS One,2016,11(3):e0149519.
[46] Ariey F,Witkowski B,Amaratunga CA,et al. A molecular marker of artemisinin-resistant Plasmodium falciparum malaria[J]. Nature,2014,505(7481):50-55.
[47] Popovici J,Kao S,Eal L,et al. Reduced polymorphism in the kelch propeller domain in Plasmodium vivax isolates from Cambodia[J]. Antimicrob Agents Chemother,2015,59(1):730-733.
[48] Talundzic E,Chenet SM,Goldman IF,et al. Genetic analysis and species specific amplification of the artemisinin resistance-associated kelch propeller domain in P. falciparum and P. vivax[J]. PLoS One,2015,10(8):e0136099.
[49] Deng S,Ruan Y,Bai Y,et al. Genetic diversity of the Pvk12 gene in Plasmodium vivax from the China-Myanmar border area[J]. Malar J,2016,15(1):528.
[50] Wang ML,Siddiqui FA,Fan Q,et al. Limited genetic diversity in the PvK12 Kelch protein in Plasmodium vivax isolates from Southeast Asia[J]. Malar J,2016,15(1):537.
[51] Brazeau NF,Hathaway N,Parobek CM,et al. Longitudinal pooled deep sequencing of the Plasmodium vivax K12 kelch gene in Cambodia reveals a lack of selection by artemisinn[J]. Am J Trop Med Hyg,2016,95(6):1409-1412.
[52] Nakeesathit S,Saralamba N,Pukrittayakamee S,et al. Limited polymorphism of the kelch propeller domain in Plasmodium malariae and P. ovale isolates from Thailand[J]. Antimicrob Agents Chemother,2016,60(7):4055-4062.
[53] Sanchez CP,Dave A,Stein WD,et al. Transporters as mediators of drug resistance in Plasmodium falciparum[J]. Int J Parasitol,2010,40(10 SI):1109-1118.
[54] Brega S,Meslin B,De Monbrison F,et al. Identification of the Plasmodium vivax mdr-like gene(pvmdr1)and analysis of singlenucleotide polymorphisms among isolates from different areas of endemicity[J]. J Infect Dis,2005,191(2):272-277.
[55] Rungsihirunrat K,Muhamad P,Chaijaroenkul W,et al. Plasmodium vivax drug resistance genes;pvmdr1 and pvcrt-o polymorphisms in relation to chloroquine sensitivity from a malaria endemic area of Thailand[J]. Korean J Parasitol,2015,53(1):43-49.
[56] Orjuela-Sanchez P,De Santana Filho FS,Chehuan YF,et al.Analysis of single-nucleotide polymorphisms in the crt-o and mdr1genes of Plasmodium vivax among chloroquine-resistant isolates from the Brazilian Amazon region[J]. Antimicrob Agents Chemother,2009,53(8):3561-3564.
[57] Musset L,Bouchaud O,Matheron S,et al. Clinical atovaquoneproguanil resistance of Plasmodium falciparum associated with cytochrome b codon 268 mutations[J]. Microb Infect,2006,8(11):2599-2604.
[58] Barton V,Fisher N,Biagini GA,et al. Inhibiting Plasmodium cytochrome bc1:a complex issue[J]. Curr Opin Chem Biol,2010,14(4):440-446.
[59] Siregar JE,Kurisu G,Kobayashi T,et al. Direct evidence for the atovaquone action on the Plasmodium cytochrome bc1 complex[J].Parasitol Int,2015,64(3):295-300.
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