抗瘧藥物通常只對部分種類的瘧原蟲有效,，這是瘧疾防治一直以來的難題。英國研究人員日前在破解這一難題方面取得進展,，他們發(fā)現(xiàn)了一種對所有惡性瘧原蟲都有效的治療途徑,。

英國桑格研究所等機構(gòu)研究人員在《自然》雜志網(wǎng)站上報告說，他們發(fā)現(xiàn)瘧原蟲在人體血液中入侵紅細胞的時候,，紅細胞上一種名為basigin的蛋白質(zhì)和瘧原蟲表面一種名為PfRh5的蛋白質(zhì)之間的聯(lián)系是至關(guān)重要的,，如果用藥物阻礙它們之間建立聯(lián)系，就可以防止瘧原蟲入侵紅細胞,，從而打斷瘧原蟲傳播瘧疾的進程。

這一發(fā)現(xiàn)的重要意義在于,，它對所有種類的惡性瘧原蟲都有效,。據(jù)介紹，瘧原蟲非常“狡詐”,，入侵紅細胞的途徑非常多樣而富于變化,，此前所發(fā)現(xiàn)的一些能防止瘧原蟲入侵紅細胞的途徑都只對部分瘧原蟲有效，而在本次研究中,，研究人員測試了所有種類的惡性瘧原蟲,，發(fā)現(xiàn)這個干預途徑對它們都有效。

研究人員加文·賴特說,，這相當于發(fā)現(xiàn)了瘧原蟲的“阿喀琉斯之踵”,，完全改變了科研人員對瘧原蟲入侵進程的看法。研究人員認為可以在此基礎(chǔ)上開發(fā)出更加有效的瘧疾防治手段,。（生物谷 Bioon.com)

doi:10.1038/nature10606
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PMID:
Basigin is a receptor essential for erythrocyte invasion by Plasmodium falciparum

Cécile Crosnier, Leyla Y. Bustamante, S. Josefin Bartholdson, Amy K. Bei, Michel Theron, Makoto Uchikawa, Souleymane Mboup, Omar Ndir, Dominic P. Kwiatkowski, Manoj T. Duraisingh, Julian C. Rayner & Gavin J. Wright

Erythrocyte invasion by Plasmodium falciparum is central to the pathogenesis of malaria. Invasion requires a series of extracellular recognition events between erythrocyte receptors and ligands on the merozoite, the invasive form of the parasite. None of the few known receptor–ligand interactions involved1, 2, 3, 4 are required in all parasite strains, indicating that the parasite is able to access multiple redundant invasion pathways5. Here, we show that we have identified a receptor–ligand pair that is essential for erythrocyte invasion in all tested P. falciparum strains. By systematically screening a library of erythrocyte proteins, we have found that the Ok blood group antigen, basigin, is a receptor for PfRh5, a parasite ligand that is essential for blood stage growth6. Erythrocyte invasion was potently inhibited by soluble basigin or by basigin knockdown, and invasion could be completely blocked using low concentrations of anti-basigin antibodies; importantly, these effects were observed across all laboratory-adapted and field strains tested. Furthermore, Oka− erythrocytes, which express a basigin variant that has a weaker binding affinity for PfRh5, had reduced invasion efficiencies. Our discovery of a cross-strain dependency on a single extracellular receptor–ligand pair for erythrocyte invasion by P. falciparum provides a focus for new anti-malarial therapies