美國哈佛大學(xué)研究人員4月21日公布研究報(bào)告稱,，他們發(fā)現(xiàn)了11個(gè)與瘧原蟲產(chǎn)生耐藥性有關(guān)的基因變異,。
研究人員在美國《公共科學(xué)圖書館—遺傳學(xué)》 PLoS Genetics 雜志網(wǎng)絡(luò)版上報(bào)告說，他們分析了來自亞洲,、非洲以及南美洲的57個(gè)已具有耐藥性的惡性瘧原蟲的脫氧核糖核酸（DNA）,，篩查了1.7萬多個(gè)基因變異，并測(cè)試了這些瘧原蟲對(duì)13種瘧疾藥的反應(yīng),，最終確認(rèn)了11個(gè)基因變異與瘧原蟲的耐藥性有關(guān),。
參與研究的哈佛大學(xué)公共衛(wèi)生學(xué)院研究人員莎拉·沃爾克曼表示，確認(rèn)與耐藥性有關(guān)的基因變異有助于理解瘧原蟲如何規(guī)避藥物作用,，并據(jù)此開發(fā)出抗瘧疾新藥,，限制瘧原蟲這種能力。
瘧疾是由瘧原蟲引起的疾病,，通過蚊子叮咬傳播,，其癥狀包括發(fā)熱、頭痛,、嘔吐等,，如不及時(shí)治療可能危及生命。在世界很多地區(qū),，瘧原蟲已經(jīng)對(duì)一些抗瘧藥物產(chǎn)生耐藥性,。據(jù)世界衛(wèi)生組織統(tǒng)計(jì)，2009年全球有78.1萬人死于瘧疾,，其中多數(shù)生活在撒哈拉沙漠以南的非洲地區(qū),。（生物谷Bioon.com）
生物谷推薦原文出處：
PLoS Genet 7(4): e1001383. doi:10.1371/journal.pgen.1001383
Identification and Functional Validation of the Novel Antimalarial Resistance Locus PF10_0355 in Plasmodium falciparum
Daria Van Tyne1#, Daniel J. Park2,3#, Stephen F. Schaffner2#, Daniel E. Neafsey2#, Elaine Angelino4,5#, Joseph F. Cortese2, Kayla G. Barnes1, David M. Rosen1, Amanda K. Lukens1, Rachel F. Daniels2,6, Danny A. Milner Jr.1, Charles A. Johnson2, Ilya Shlyakhter2,3,4, Sharon R. Grossman2,3,4,5, Justin S. Becker1, Daniel Yamins4, Elinor K. Karlsson2,3,4, Daouda Ndiaye7, Ousmane Sarr7, Souleymane Mboup7, Christian Happi8, Nicholas A. Furlotte9, Eleazar Eskin9, Hyun Min Kang10, Daniel L. Hartl3, Bruce
The Plasmodium falciparum parasite's ability to adapt to environmental pressures, such as the human immune system and antimalarial drugs, makes malaria an enduring burden to public health. Understanding the genetic basis of these adaptations is critical to intervening successfully against malaria. To that end, we created a high-density genotyping array that assays over 17,000 single nucleotide polymorphisms (~1 SNP/kb), and applied it to 57 culture-adapted parasites from three continents. We characterized genome-wide genetic diversity within and between populations and identified numerous loci with signals of natural selection, suggesting their role in recent adaptation. In addition, we performed a genome-wide association study (GWAS), searching for loci correlated with resistance to thirteen antimalarials; we detected both known and novel resistance loci, including a new halofantrine resistance locus, PF10_0355. Through functional testing we demonstrated that PF10_0355 overexpression decreases sensitivity to halofantrine, mefloquine, and lumefantrine, but not to structurally unrelated antimalarials, and that increased gene copy number mediates resistance. Our GWAS and follow-on functional validation demonstrate the potential of genome-wide studies to elucidate functionally important loci in the malaria parasite genome.
